Communicable Disease Nursing: Mrs. Dionesia Mondejar Navales

Download as ppt, pdf, or txt
Download as ppt, pdf, or txt
You are on page 1of 64

COMMUNICABLE

DISEASE NURSING

Mrs. Dionesia Mondejar Navales


Definition Of Common Terminologies:
Communicable Diseases – are diseases that are transmitted from
one person to another directly or indirectly.

Infectious Diseases – requires direct inoculation of microorganism


of microorganism to produce a disease

Contagious Diseases – are diseases that are easily transmitted


from one person to another by direct or indirect means

Epidemiology – that branch of medical science which deals


on the causes, occurrence, and distribution of disease,
disability , and death among groups of people.
a. epidemic
b. endemic
c. pandemic
d. sporadic
Triad of Epidemiology

Factors Affecting The Acquisition Of Organism


Host
• Patient
• Carrier
• Contact
• Suspect

Agents
1. Virus
a. Smallest microorganism
b. Attack both living and non-living organism
c. Usually has longer incubation period
d. Person acquire longer or lifetime immunity
e. Self-limiting

2. Bacteria
a. Attack both living and non-living organism
b. Usually has shorter incubation period
c. Short or no immunity acquired
d. Bacterial infection can be treated easily due to the advent of
antibiotics
3. Rickettsia
a. Unable to grow on artificial media
b. All rickettsial diseases are transmitted by arthropods (ticks, flea,
mites, lice)
c. Require living cell for growth and multiplication
4. Spirochete
a. Spiral-shape bacteria
b. Move in an spiral, helical, or inch-worm manner (leptospira)

5. Chlamydia - usually are transmitted through sexual contact


6. Fungi – some are harmful, some are beneficial .
7. Protozoa
•Single-celled organism
•Composed of two stages;
a) Throphozoite is the motile, feeding, and dividing stage of life cycle
b) Cyst- the dormant, survival stage

8. Parasites – usually lives in the expense of others.


For the organism to cause a disease, it should posses the following;
1. Pathogenicity
2. Virulence
3. Invasiveness
4. Infective dose
5. Elaboration of toxin
Environment:
Should be favorable for the growth and multiplication of microorganisms.1

CHAIN OF INFECTION

Infection – is the implantation and successful replication of the


organisms in the tissue of the host.
Chain of Infection Diagram
1. Agent
2. Reservoir
a. Human
· Frank cases – the very ill
· Sub-clinical/ambulatory
· Carrier
b. Animals
c. Non-living

3. Portals of Exit (GIT, GUT. Respiratory. Integumentary)


4. Mode of transmission
a. Contact transmission
b. Airborne
c. Vehicle borne
d. Vector borne

5. Portals of entry
6. Susceptible host
Factors in consider in the host’s resistance;
1. Skin and mucous membrane
2. Humoral immune response
3. Cell-mediated immune response

Immunity – free from any particular disease


1. Natural or inherent
a. Natural active – participation of the body in the acquisation of immunity
b. Natural passive – acquired through placental transfer
2. Artificially acquired
a. Active – gained through administration of toxoid
b. Passive – gained through administration of anti-toxin, anti-serum.
This elicit immediate action
Vaccines:
1. Attenuated (live organism)
· Single dose
· Lasting immunity
2. Inactivated (killed organism)
· Requires multiple doses
· Booster dose needed to confirm immunity
Aspects Of Care of a CD Patient
1. Preventive aspect
· Health education
· Immunization
2. Control system
· Isolation
· Quarantine
· Disinfection
♠ Concurrent
♠ Terminal
· Disinfestation
· Fumigation
· Use of PPE
· Universal/Standard precaution
3. Curative
· Medical management
· Nursing management
4. Rehabilitative
· Activity
· Nutrition
DISEASES AFFECTING THE
CENTRAL
NERVOUS SYSTEM
Tetanus
(Lockjaw)

- An infectious disease affecting the CNS usually manifested by generalized


spasmodic contractions of the skeletal musculator
- Incubation period; 3 days – 3 weeks in adult, 3 – 30 days in neonate
- Etiologic agent is Clostridium tetany with the following characteristics;

•Anaerobic, gram (+) spore former, drumstick in appearance


•Comes in two forms, spore forming & vegetative
•Releases two types of toxin; Tetanolysin – responsible for RBC destruction,
and tetanospasmin – responsible for muscular spasm. Next to Botulinus,
these toxin is known to be the most lethal toxin to man
•Habitat is the intestinal wall of grass-eating animals

Avenues for entrance of the organism;


● Rugged traumatic wounds and burns
● Umbilical stump
● unrecognized wounds
● Dental extraction, circumcision, ear piercing
Pathogenesis:
- Clostridium tetani enters the body, produce local infection and
tissue necrosis
- While reproducing, release toxin, absorbed by the bloodstream
and the lymphatics, spread to the CNS to the anterior horn cells
of the spinal cord, thus, stimulate contraction of the muscles
supplied by the neurons to which toxin difuses.

Clinical Manifestations:
A. Neonate
ü Feeding and sucking difficulty
ü Excessive crying
ü Spasm and cyanosis
ü Muscular spasm provoked by stimuli
ü Cyanosis and pallor
ü Exhaustion
ü DEATH
B. Older children and adults:
1. Increase muscle tone near the wound it tetanus remain localized
2. If it become systemic,
a) Low grade fever and painful involuntary muscle contraction
b) Trismus
c) Risus sardonicus
d) Abdominal rigidity
e) Opisthotonos
f) Intermittent clonic and tonic convulsions resulting to sudden death
due to asphyxation
g) Laryngospasm
3. In mild cases, after a period of weeks, spasm diminishes in frequency and
severity, with trismus being the last symptom to disappear.
4. In fatal cases, death usually occurs during the first 10 days of the disease

Complications:
1. Respiratory
a) Hypostatic pneumonia
b) Hypoxia due to laryngospasm
c) Atelectasis
d) Pneumothorax
2. Due to trauma
a) Laceration of the tongue and bucal mucosa
b) Intramuscular hemtoma
c ) Fracture of the ribs and the spine due to prolong opisthotonos
3. Septicemia

Baby infected with Tetanus


Treatment:
1. Specific
a) ATS, TAT, and TIG should be given 7within 72 hours after injury
b) Tetanus toxoid given in regular schedule
c) Antibiotics to control infection
d) Adequate fluid, electrolyte and caloric intake
e) Good nursing care
ü Avoidance of external stimulation
ü Prevention from further injury
ü Maintain adequate airway
ü Maintain an IV line for medication and emergency care if necessary
ü Carry out efficient wound care
ü Avoid contractures and pressure sores
ü Watch for urinary retention
ü Close monitoring of vital signs and muscle tone
ü Provision of optimum comfort measures

Prevention and Control:


1. Active immunization with Tetanus toxoid in adult
2. DPT for babies and children
3. Early consultation and adequate wound care after an injury
Meningitis
(Cerebrospinal fever)

Ø The inflammation of the meninges of the brain and the spinal


cord.
Ø Caused by several organisms which include; pneumococcus,
staphylococcus, streptococcus, and tubercle bacillus. Neisseria
meningitides (meningococcus) is the organism causing most
epidemics of meningitis.
Ø Incubation period : 1 – 10 days.
Ø Mode of transmission :
ü Respiratory droplet
ü Direct invasion through oitis media
ü Skull fracture, penetrating head injury
ü Complication of an existing viral disease
Ø Diagnostic Tests:
a.) CSF analysis ( lumbar puncture)

Purposes of Lumbar puncture:


1. Diagnostic
ü To obtain specimen (CSF)
ü To take x-ray of the spinal canal
2. Therapeutic
ü To reduce intra-cranial pressure
ü To introduce medication
ü To inject anesthetic agent

b) Gram staining
c) Smear and blood culture
c) Urine culture
Types of Meningitis:
1. Aseptic meningitis
Ø Begin with benign syndrome characterized headache, fever,
vomiting and meningeal symptoms
ü Stiff neck or nuchal rigidity
ü Opisthotonos
ü (+) Brudzinski
ü (+) Kernig
Ø Sinus arrythmia, irritability, photophobia, diplopia and other visual
problems
Ø Abnormal movements of the extremities, spasm, decortication,
descerebrate
Ø Delirium, deep stupor, coma
Ø Signs of intracranial pressure:
ü Bulging fontanel in infants
ü Nausea and vomiting (projectile)
ü Severe frontal headache
ü Blurring of vision
ü Alteration in sensorium

Complications:
Ø Subdural effusion
Ø Hydrocephalus
Ø Deaf-mutism
Ø Blindness
Ø Otitis media and mastoiditis
Ø Pneumonia and bronchitis
Modalities of treatment:
Ø If left untreated, mortality rate 70 – 100%
Ø Antibiotics (Ceftriaxone) to control infection
Ø Digitalis (Digoxin) to control arrythmias
Ø Manitol (diuretics) to control edema
Ø Anticonvulsants to reduce restlessness and convulsions
Ø Acetaminophen to relieve headache and fever
Nursing Management:
Ø Assess neurologic condition of patient
Ø Observe level of consciousness
Ø Check for signs of ICP
ü Plucking at bedcovers
ü Projectile vomiting
ü Seizures
ü Change in motor functions and vital signs
Ø Maintain adequate fluid intake to avoid dehydration but avoid fluid
overload to prevent cerebral edema
Ø Correct positioning to prevent deformities, pressure sores and
respiratory complications
Ø Maintain adequate nutrition and elemination
Ø Isolation
Ø Provide reassurance to patient and the family
2. Acute meningococcemia (Spotted fever)
Ø Most common among children ages 6 months to 5 years
Ø Following an incubation period of 3 – 5 days, meningococci invade the
bloodstream, the joints, the skin, the adrenals, and the lungs without
involving the meninges.
Ø Manifestations start with nasopharyngitis followed by sudden onset of
spiking fever with chills, nausea, vomiting, malaise, and headache
Ø Petechiae, purpura, ecchymotic hemorrhages scaterred all over the
body and mucous membrane
Ø Adrenal lesions start to bleed into the medulla which extends into
the cortex
Ø Dermal manifestations and adrenal hemorrhages is known as
Waterhause-Friderichen syndrome

Types of meningococcemia:
a) Fulminant – the rapid development of petechiae, purpuric, ecchymotic
spots associated with shock. The condition runs short and usually fatal.

b) Non-fulminant – transition of lesions is delayed and chance for survival


is 85%.
Opisthotonus

Decortication
Meningococcemia
Nursing Management:
Ø Isolation
Ø Strict aseptic technique
Ø Emotional support

Prevention:

Ø Immunization. (Polysaccharide vaccines)


ü Monovalent A
ü MonovalentC
ü Bivalent AC
Ø Prompt medical treatment and diagnosis
Ø Rifampicin as prophylaxis
Encephalitis
(Brain fever)
Ø An acute inflammatory condition of the brain usually occurring as a
complication or sequel to some viral diseases
Ø Caused by a variety of pathologic agents, like bacteria, viruses, fungi,
rikettsia, toxins, chemical, substances, or trauma.
Ø Incubation period is 5 – 15 days
Ø Classifications:

1. Primary – caused by direct inhalation of noxious substances;


- direct invasion of the CNS by arthropods.
a. Eastern Equine Encephalitis
ü Principally affecting children below 5 years old
ü Harbored by Aedes sulicitans mosquito
b. Western Equine Encephalitis – milder type and usually
affecting adults.
c. St. Louise Encephalitis
ü Usually harbored by mosquito Culex tarsalis
ü Organism is believed to gain entrance through the
olfactory tract
d. Japanese Encephalitis
ü Disease is spread by mosquito Culex triteaniorhynchus that live in rice-
growing and hog-raising areas
ü Once mosquito is infected, it is capable of transmitting the disease
for life
ü Usually affecting children 5 – 10 years old, more in male than in female
with a ratio of 3 : 1
ü Peak season for JE is March – April; September – October where rice
field is flooded
2. Secondary Encephalitis
a) Post infection – usually post viral infection
b) Post vaccinal – most common is anti-rabies vaccine
Clinical Manifestations:
1) Fever, headache, dizziness, vomiting, and apathy
2) Chills, sore throat, conjunctivitis, artharlgia, myalgia, and abdominal pain
3) Ocular palsy, ptois, and flccid paralysis
4) Disturbances in swallowing, mastication, phonation, respiration and
movements of the muscles of the eyes or face
5) Uncontrollable contraction or twitching of the muscles of the different parts
of the body
6) Encephalitic signs manifested by nuchal rigidity, ataxia, tremors, mental
confusion, speech difficulties, stupor, hyperexcitability, convulsions, coma,
and DEATH
Diagnostic Tests
1) EEG
2) CSF analysis
3) Serologic test – 90% confirmatory
4) ELISA

Sequelae:
1) Motor disturbance
ü Persistent convulsion
ü Parkinsonian syndrome or Paralysis agitans
ü Epilepsy-like manifestaion
2) Mental Disturbances
ü Mental dullness
ü Mental deterioration
ü Lethargy
ü Mental depression
ü Sleep disturbance
3) Endocrine disturbances
ü Patient may grow fat or thin
ü In adult, sexual interest or activity is lost
Nursing Management:

ü Symptomatic and supportive


ü Control of convulsions
ü Sanitary disposal of nose and throat secretions
ü Unless patient is comatose, patient is encouraged oral fluid intake
ü Provide safety
ü Intake and output should be closely monitored
ü Observe for neurologic signs involving speech, swallowing difficulty
of speech
ü Frequency and duration of convulsions should be observed

Prevention and Control:

1. Elimination of breeding places


2. Destruction of larvae
3. Screening of houses
4. Use of repellents
5. Health education, information dissemination
Rabies
(Hydrophobia; Lyssa)
Ø A specific, viral infection communicated to man by an infected animal
Ø Caused by a bullet shape organism that has an affinity to the CNS
Ø The organism is resistant to phenol, merthiolate, and common
antibacterial agents
Ø Recommended first aid is to wash the wound with soap and water
for about 3 minutes and apply tincture of iodine
Ø Incubation period is 1 week – 7 months in dogs; and 10 days to
15 years in human
Ø Incubation period depends upon 5 factors;
ü Distance of the bite to the brain
ü Extensiveness of the bite
ü Specie of the biting animal
ü Richness to nerve and blood supply
ü Resistance of the host
Ø Patient is communicable 3 – 5 days before onset of symptoms until
the entire course of illness
Pathogenesis:
Clinical Manifestation:
1. Prodromal/invaion phase
ü Fever, anorexia, malaise, sore throat, lacrimation, irritability,
hyperexcitability, apprehensiveness, restlessness, mental depression
ü Numbness, pain, and tingling sensation at the site of the bite felt
along the peripheral nerves
2. Excitement/Neurological phase
ü Marked excitation, apprehension, and terror may occur
ü Delirium, associated with nuchal rigidity, generalized muscular
twitching and convulsions
ü Maniacal behavior, skin cold and clammy
ü Painful spasm of the muscles of the mouth, pharynx, larynx on
attempt to swallow water or even at the mere sight of them
ü Aerophobia
ü Frothy saliva drools from the mouth of the patient’s mouth
ü DEATH may occur during the episodes of spasm
3. Terminal /Paralytic phase
ü Patient becomes quiet and unconscious
ü Loss of bowel and urinary control
ü Spasm ceases with progressive paralysis
ü Tachycardia, labored, and irregular respiration
ü DEATH occurs due to respiratory and circulatory collapse
Diagnostic Tests:
1. Virus isolation from the patient’s saliva and throat
2. Fluorescent rabies-antibody (FRA) – provides the most definitive diagnosis
3. Presence of negri bodies in the dog’s brain

Treatment Modalities:
1. Thoroughly wash wound with soap and water
2. Immunization/vaccination
3 ATS/TAT infiltrated around the wound or IM ANST
4. Anti-rabies vaccine, both passive and active
Schedule of Vaccination (Adopted from SLH)
A. Passive
1. ERIG - P
2. ERIG – B
3. HRIG
B. Active
1) Standard Regimen

Verorab Rabiphur
D0 ..1cc x 2 sites . 2cc x sites ID Deltoid
D3 . 1 cc x 2 sites .2cc x 2 sites ID Deltoid
D7 .1 cc x 2 sites .2 cc x 2 sites ID Deltoid
D28 . 1 cc x 1 site .2 cc x 1 site ID Deltoid
D90 . 1 cc x 1 site . 2 cc x 1 site ID Deltoid
2) Special Regimen: (2 – 1 – 1)

D0 1 vial x 2 sites IM Deltoid


D7 1 vial x 1 site IM Deltoid
D14 1 vial x 1 site IM Deltoid

Prevention:
1. Vaccination of all dogs
2. Enforcement of the regulation regarding stray dogs
3. Public education in avoiding or reporting all animals that appear
week.
DISEASES AFFECTING
THE
GATROINTESTINAL TRACT
(GIT)
TYPHOID FEVER
Ø A bacterial infection of the GIT affecting the lymphoid tissues
(Peyer’s Patches) of the small intestines
Ø Caused by an organism Salmonella typhosa/typhi, a gran negative,
non-spore forming, pathogenic to man only
Ø Incubation Period is 5 – 40 days
Ø Period of Communicability: Variable

Sources of Infection

ü Carriers – could be one who recovered from the disease or one who
have cared for a patient with Typhoid and was infected.
ü Ingestion of shellfish (oysters) taken from waters contaminated by
sewage disposal
ü Stool and vomitus of infected individual
Mode of Transmission
· Fecal-oral transmission
· Organism can be transmitted through the five (5) F’s
· Ingestion of contaminated food, water and milk

Pathogenesis
I. Typhoid Ileitis

Salmonella thyphi

Bowel (Peyer’s patches)

Lymph nodes are swollen

Pus formation; necrosis

Tissue slough off leaving ulcerated surface

Hemorrhage and perforation (melena)

Peritonitis & Toxemia

Heart, spleen, liver, mesynteric lymph nodes are red and swollen
Clinical Manifestations

I. Onset
· Headache, chilly sensation, aching all over the body,
· Nausea, vomiting and diarrhea
· By the 4th and 5th day all symptoms are worst
· Fever is higher in the morning than it was in the afternoon.
Temperature graph appears “ladder – like or stairway”
· Breathing is accelerated, the tongue is furred, the skin is dry
and hot, abdomen is distended and tender
· Rose spots appear on the abdominal wall on the 7th to the 9th day
· On the second week symptoms become more aggravated.
Temperature remains in uniform level. Rose spots become more
prominent.
II. Typhoid State
· Intense symptoms decline in severity
· The tongue protrudes, become dry and brown
· Teeth and lips accumulate a dirty-brown collection of dried
mucus and bacteria known as sordes.
· Coma vigil
· Subsultus tendinum
· Carphologia
· There is constant tendency for the patient to slip down to the foot
part of the bed
· In severe cases rambling delirium sets in often ending in coma & death

Complications
· Bronchitis and pneumonia
· Meteorism or excessive distention of the bowels (Tympanites)
· Thrombosis and embolism
· Early heart failure
· “Typhoid spine” or neuritis
· Septicemia
· Reiter”s syndrome – joint pain, eye irritation, painful urination that
can led to chronic arthritis
Diagnostic Procedure
· SEIA – Salmonella Enzyme Immuno-Assay
· Typhidot
· ELISA
· Widal test
· Rectal swab

Modalities of Treatment
· Chloramphenicol – drug of choice
· Ampicillin
· Co-trimoxazole
· Ciprofloxacin or Ciftriaxone

Nursing Management
· Maintain or restore fluid and electrolyte balance
· Monitor patient’s vital signs
· Prevent from further injury (fall) in patient with typhoid psychosis
· Maintain good personal hygiene and mouth care
· Cooling measures during febrile state
· Watch for signs of intestinal bleeding
Prevention and Control

· Sanitary/proper disposal of excreta


· Proper supervision of food handlers
· Enteric isolation
· Adequate protection or provision of safe drinking water supply
· Reporting of cases to health authorities
VECTOR – BORNE
DISEASES
DENGUE FEVER
(Breakbone Fever)

Ø An acute febrile disease caused by Dengue virus which are transmitted


by a mosquito Aedes egypti with the following characteristics:
ü Day-biting (2 hours after sunrise and 2 hrs before sunset)
ü Breeds on stagnant water
ü Limited movement and usually low-flying
ü Fine dots at the base of the wings with white bands
Ø Incubation period: 3 – 14 days
Ø Patient is infective to mosquito from a day before the febrile period to
the end
Ø Mosquito become infective from day 8 – 12 after blood meal and remains
infective through out life
Ø Pathognomonic sign: Herman’s sign (Extravasation of blood in petechiae)
Clinical Manifestations:
I. Dengue fever
· Fever and chills associated by severe frontal headache, ocular pain,
myalgia with severe backache, and arthralgia
· Nausea and vomiting
· Fever is non-remitting and persist for 3 – 7 days
· Rash is more prominent on the extremities and the trunk. It may
involve the face in some isolated case
· Petechiae usually appear near the end of the febrile period and
most common on the lower extremities.

II. Dengue Hemorrhagic Fever (DHF)

This severe form of dengue virus infection is manifested by fever,


hemorrhagic diathesis, hepatomegally and hypovolemic shock.
Phases of the Illness:
1. Initial febrile phase lasting from 2 – 3 days
· fever (39 –40 ºC) accompanied by headache
· palms and sole are usually flushed
· positive tourniquet test
· anorexia, vomiting, myalgias
· Appearance of Herman’s sign known as pathognomonic to the disease.that
usually start from the distal portion of the body
· Generalized or abdominal pain
· Hemorrhagic manifestations, like positive tourniquet test, purpura, epistaxis
and gum bleeding maybe present

2. Circulatory phase
· fall of temperature accompanied by profound circulatory changes usually on
the 3rd – 5th day
· patient become restless, with cool clammy skin
· profound thrombocytopenia accompanies the onset of shock
· bleeding diathesis may become more severe with GIT hemorrhage
· shock may occur due to loss of plasma from the intravascular
spaces and hemoconcentration with markedly elevated hematocrit is present
· pulse is rapid and weak; pulse pressure become narrow and blood pressure
may drop to an unobtainable level
· untreated shock may result to comma, metabolic acidosis and death may
occur within 2 – days.
· With effective therapy, recovery may follow in 2 – 3 days.
Classification According to Severity (Halstead & Nimmanitya)

Grade I
Fever accompanied by non-specific constitutional symptoms and the only
hemorrhagic manifestation is positive (+) tourniquet test.
Grade II
All signs of grade I plus spontaneous bleeding from the nose, gums, GIT
Grade III
Presence of circulatory failure as manifested by weak pulse, narrow pulse
pressure, hypotension, cold clammy skin and restlessness
Grade IV
Profound shock, undetectable blood pressure and pulse

Complications:

1. Dengue Fever
1. Epistaxis; menorrhagia
2. Gastrointestinal bleeding
3. Concomitant gastrointestinal disorder (peptic ulcer)
2. D H F
1. Metabolic acidosis
2. Hyperkalemia
3. Tissue anoxia
4. Hemorrhage into the CNS or adrenal glands
5. Uterine bleeding may occur
6. Myocarditis

3. Severe manifestations
1. Dengue encephalopathy – manifested by increasing restlessness,
apprehension or anxiety, disturbed sensorium, convulsions, spacity,
and hyporeflexia

Diagnostic Tests:
1. Tourniquet test – screening test, done by occluding the arm veins for
about 5 minutes to detect capillary fragility
2. Platelet count (decreased) – confirmatory test
3. Hemoconcentration – an increase in at least 20% in hematocrit or
steady rise in hemartocrit
4. Occult blood
5. Hemoglobin determination
Treatment Modalities:
There is no effective anti-viral therapy for dengue fever. Treatment is
entirely symptomatic;
1. Analgesic drugs other than aspirin maybe required for relief of
headache, ocular pain, and myalgia.
2. Initial phase may require intravenous infusion to prevent from
dehydration and replacement of plasma.
3. Blood transfusion is indicated in patient with severe bleeding
4. Oxygen therapy is indicated to all patients in shock
5. Sedatives maybe needed to allay anxiety and apprehension

Nursing Management:
1. Patient should be kept in mosquito-free environment to avoid further
transmission of infection
2. Keep patient at rest during bleeding episodes
3. Prompt monitoring of vital signs
4. For nose bleeding, maintain patient’s position in elevated trunk, apply
ice bag to bridge of nose and to the forehead.
5. Observe signs of shock, such as slow pulse, cold clammy skin,
and fall of BP
6. Restore blood volume, put patient in Trendelenberg position to provide
greater blood volume to the head part
Prevention and Control:
1. Early detection and treatment of cases
2. Insecticide treatment of mosquito nets
3. House spraying
4. Implementation of 4 o’clock habit
5. Avoid too many hanging clothes inside the house

Four “S” in Dengue (Adopted From DOH)

1. Search and destroy


2.Self protection measures
3. Seek early consultation
4. Say NO to indiscriminate fogging
MALARIA
(Ague)

 An acute and chronic parasitic disease transmitted by the bite of


infected female Anopheles mosquitoes .
 Etiologic agent is a protozoa of genus plasmodia

1.Plasmodium falciparum (malignant tertian)


 considered as the most serious malarial infection

2.Plasmodium vivax (Benign tertian)

 manifested by chills every 48 hours on the 3rd day onward


especially if untreated

3.Plasmodium malariae (Quartan)


 fever and chills usually occur on the 4th day after onset
 non-life threatening

4.Plasmodium ovale – the rare type


Anopheles mosquito has the following characteristics
 breeds in clear, flowing, and shaded streams usually in the mountains
 they are brownish in color and bigger in size than the ordinary mosquitoes
 they are the night-biting mosquitoes
 usually don’t bite a person in motion
 assumes a 36º position when they alight on walls, trees, curtains, etc.

Incubation period
 12 days for P. Falciparum
 14 days for P. vivax and ovale
 30 days for malariae

Period of Communicability
 Untreated or insufficiently treated patient may be source of mosquito
nfection for more than 3 years in P. malariae; 1 – 2 years in P. vivax,
and not more than one year on P. falciparum.
Mode of Transmission
 Mechanical, through bite of an infected female anopheles mosquito
 Parenteral, through blood transfusion
 In rare occasion, from shared contaminated needles
 Transplacental, congenital malaria; a rare case

Clinical Manifestations
 Paroxysms of shaking chills
 Rapidly rising fever with severe headache
 Profuse sweating
 Myalgia, with feeling of well-being in between
 Splenomegally, hepatomegally
 Orthostatic hypotension
 Paroxysms may last for 12 hours, then, maybe repeated daily or after
a day or two
 In children;
= fever maybe continuous
= convulsions and gastrointestinal symptoms are prominent
= splenomegally
 In cerebral malaria
= changes in sersorium, severe headache, and vomiting
=Jacksonian or grand mal seizure may occur
Diagnostic Procedure

 Malarial smear – a film of blood is placed on a slide, stained and


examined microscopically

 Rapid diagnostic test (RDT) – are blood tests for malaria that can be
conducted outside the laboratory and in the field, giving a result within
10 – 15 minutes. This is done to detect malarial parasite antigen in the blood.

Means of propagation:
1. Sexual – takes place in the stomach of man
2. Asexual – takes place in the RBC of man
Management

1. Medical
· Anti-malarial drugs
= Chloroquine (all species except for P. malariae)
= Quinine
= Sulfadoxine for resistant P. falciparum
= Primaquine – for relapse of P. vivax and ovale

Antimalarial drugs currently used for treatment

• Mefloquine
• Chloroquine
• Amodiaquine
• Quinine/Quinidine
• Atovaquone
2. Nursing Management

· Close monitoring of patient


· Strict monitoring of intake and output to prevent pulmonary edema
ü daily monitoring of patient’s serum bilirubin, BUN creatinine, and
parasitic count
ü if with respiratory and renal symptoms, determine arterial blood
gas and plasma electrolyte
· When the patient is chilling, keep him warm
· During the febrile stage, tepid sponges, alcohol rubs, ice cap on the
head will help bring down the temperature
· Encourage patient to take plenty of fluids
· Bed and clothing should be kept dry
· Provide psychological and spiritual support
Prevention
1. Reporting of malaria cases
2. Destruction of breeding places
3. Spraying homes with effective insecticides with residual actions
on the wall
4. Use of mosquito nets
5. Proper screening of blood donors
6. People living in malaria-infected areas should not donate blood
for at least 3 years
FILARIASIS
(Elephantiasis)
 An extremely debilitating and stigmatizing disease caused by parasitic
worms, Wuchereria bancrofti, a 4-5 cm long thread-like worms that
affect the body’s lymph nodes and lymph vessels
 The disease is transferred from person to person by mosquito bites,
Culex tarsalis which is active during the night time to dawn

• The microscopic worms pass from the mosquito through the skin and travel
to the lymph vessels where they grow into adults, and live in 7 years in the
lymph vessels
 The disease damage the kidneys and the lymph system; fluid collects
and causes swelling in the arms, breasts, legs, and for men, the genital area.
 A person with this disease tend to have more bacterial infections in the
skin, thus, causes hardening and thickening of the skin, which
is called elephantiasis.
 In conjunctival filariasis, the worms’ larvae migrate to the eye and
sometimes can be seen beneath the conjunctivae, that can lead to
blindness known as onchoceriasis
Symptoms:
· Infections usually begin with chills, headache, and fever between
three months and one year after the insect bite.
· There may also be swelling, redness, and pain in the arms, legs, or
scrotum.
· Areas of abscesses may appear as a result of dying worms or a
secondary bacterial infection.

Complications
1. Recurring infections, fevers, severe inflammation of the lymph system
2. Lung condition called Tropical Pulmonary Eosinophilia (TPE).
3. The legs become grossly swollen .that can lead to severe disfigurement,
decreased mobility, and long-term disability.
4.Testicular hydrocele is a disfiguring enlargement of the scrotum.
Diagnostic Procedures:
· Circulating Filarial Antigen (CFA) test – performed on a finger-prick
blood droplet taken any time of the day and gives result in a few minutes

Modalities of Treatment.
1. Ivermectin,
2. Albendazole, or
3..Diethylcarbamazine (DEC) – used to treat by;
· Eliminating the larvae
· Impairing the adult worms ability to reproduce
· By actually killing the adult worms
LEPTOSPIROSIS
Mode of Transmission

 Ingestion or contact with the skin and mucous membrane with the infected
urine or carcasses of wild and domestic animals
 Through the mucous membrane of the eyes, nose, and mouth, and
through a break on the skin
 Leptospira enters the blood stream to cause damage on the kidneys,
the liver, meninges and conjunctivae.

Clinical Manifestations

1. The symptoms range from severe to asymptomatic fatal outcome


2. Clinical course is generally biphasic and the majority of the cases are
unicteric. In icteric cases, typical color of the eyes is- orange
3 Three stages can be recognized:

 Septic stage –. There is an abrupt onset of remittent fever, chills,


headache, anorexia, abdominal pain, and severe prostration and
respiratory distress.

 Immune or toxic stage –


 Iritis, headache, meningeal manifestations like disorientation,
convulsions wit CSF findings of aseptic meningitis
 Oliguria and anuria with progressive renal failure
 Shock, coma, and congestive heart failure. Death may occur between
the 9th to the 16th day

 Convalescence - relapse may occur during he 4th to 5th week


Management
1. Medical
a. Penicillin G Na
b Tetracycline
a. Peritoneal dialysis
b. Administration of fluid and electrolyte and blood as indicated

2. Nursing
a. Isolate the patient, urine must be properly disposed
b. For home care, cleaning near dirty places, pools, and stagnant water
c. Eradicate rats and rodents

Prevention and control

a. Sanitation in homes, workplaces, and farms


b. Proper drainage system and control of rodents (40 – 60% infected)
c. Vaccination of animals (cattle, dog, cats and pigs)
d. Treatment of infected human and pets
e. Effective information- dissemination campaign

You might also like