Module on Communicable Diseases

Community Health Nursing is faced with problems regarding communicable diseases. It is important therefore that the nurse poses basic
knowledge on how to deal with related problems and more so prevent its occurrence, since this is likewise the focus of community health
nursing.
INTRODUCTION
This module focuses on the basic communicable diseases affecting the patterns of mortality and morbidity in the Philippine community. It
will give you the basic information regarding the description, etiology, mode of transmission, incubation period, signs and symptoms,
diagnostic procedures and management of these diseases. As an added bonus each topic is carefully selected to prepare you both in the
practical application in the community setting and the board exam most especially. Due to this you are advised to be familiarized with the
following phrases:
ON THE BOARD refers to common question that comes out in the board exam.
CLINICAL FOCUS refers to the important reminders that are crucial in the actual practice.
GROUP ALERT refers to age group variation that also demand different approaches. A post test is prepared for your satisfaction so that you
will be able to measure your knowledge. It is recommended that you supplement your studies with text books which focus on the said topic.
This is just a guide and although careful review has been made the author waive any responsibility that may negatively occur due to
application of the concepts learned here in.
OBJECTIVE GENERAL To study the different communicable diseases affecting man and the family as a component of the community
SPECIFIC By the end of the module in 7 days you should be able to;
1. Understand the basic concepts of CD
2. Familiarize with the basic control and method of prevention to the said diseases.
3. be able to apply to practice the concepts learned by effectively giving health education all these is expected to be attained by you none the
less, by passing at least 65% of the final assessment questions.
What is infection? Infection is the successful entry and multiplication of micro-organism in the human body. Usually their entrance results
in the appearance of the disease. But it doesnt always follow the same. Some organism may enter the body but no obvious illness is
apparent.
What are the types of infection? There are two types of infection it could be nosocomial or opportunistic. Nosocomial refers to hospital
acquired infection with sets in within the premises of the hospital during confinement. Remember an infection is considered nosocomial if it
sets in after 72 hours upon admission. Most of the time the responsible organism are hospital pathogens such as pseudomonas, klebsiella
etc. Opportunistic refers to the type infection acquired due to the failure of the immune defenses. Usually this is caused by the normal
microflora.
What are communicable diseases and contagious diseases? Communicable diseases are any disease that are caused by microorganism
and can be transferred from one body to another, hence it is communicable. Contagious diseases are any communicable infection that are
easily transmissible. ON THE BOARD! Keep in mind that every contagious disease is communicable and all communicable diseases are
infection but never the other way around.
What is pathogenicity? It is the over all ability of the organism to cause pathogenic changes in the body. Which is further described by the
following terms:
Mode of action manner by which organism damages the host. Example clostridium tetani releases toxin while plasmodium falciparum
kills the RBC.
Virulence it is the over all strength of the microorganism
Dose the number of the organism required to cause infection for example as little as 4 tubercle bacilli inhaled is sufficient to
cause Tuberculosis among high risk patient. Invasiveness the ability of the organism to penetrate an intact barrier
Toxigenicity the ability of the organism to produce toxins
Specificity is the ability of the organism to attach on specific cellular surface receptors. Viability the ability to sustain life outside the
body of the host
Antigenicity the ability of the organism to stimulate and or resist antibody response
THE 3 LEVELS OF PREVENTION
PRIMARY focuses on health promotion and disease prevention
Promotive there is no risk of having the disease. Activity is directed in promoting healthy lifestyle, proper nutrition, adequate exercise and
environmental sanitation.
Preventive risk of having the disease is already existing and activity is directed in avoiding the risk ergo the disease it self. Example are
EPI, Pap smear, BSE and STE.
SECONDARY focuses on the Curative aspect of care.
Curative effort is directed for early treatment. Move is also undertaken to avoid possible complications
TERTIARY focuses on the rehabilitative aspect
Rehabilitative effort of helping the patient adjust with the limitations and disability brought about by the previous disease.
ELEMENTS OF DISEASE CAUSATION Refers to the relationship of the Agent (microorganism), Host (Human) and the Environment
(reservoir). If balance between the three is present disease is absent but if one of the three gain advantage over the other it may compromise
one element and cause disease.
STAGES OF INFECTION
a) Exposure the stage of contact with the infectious agent
b) Incubation or latent the organism successfully entered the body. No apparent illness is present. The organism is still multiplying so as to
manifest an actual illness.
c) Prodromal the manifestation of vague signs and symptoms start to appear. Example fever, cough, pain etc.
d) Acute disease an acute disruption in the physiologic mechanism. Disease due to the infecting organism is already present.
e) Convalescence the stage of resolution. The body is able to maintain homeostasis. The infectious organism is under control
f) Relapse a stage of reactivation of a previous infection which may be due to re-exposure or waning immunity.
CHAIN OF INFECTION The series of events that takes place in order for infection to occur.
The following subtopics describe each component of the chain.
ON THE BOARD! Remember infection will never occur unless the six chain are completed.
a) Causative agent refers to the microorganism such as fungi, protozoa, parasite, viruses, bacteria etc.
b) Reservoir the medium or body which the microorganism thrive and survive.
c) Portal of Entry opening in the body where in the microorganism could use as passageway to reach the internal physiological structures.
For example mouth, nose, wound etc.
d) Portal of exit any opening to which the organism uses to exit from the body. Example are anus, nose, vagina, penis, etc.
e) Mode of transmission the method on how the organism travels from one infected host to another.
i. Direct requires physical contact from the point source of infection. Such as kissing and unprotected sexual intercourse.
ii. Indirect transmitted through fomites and other non living organism. Contaminated surgical instruments.
iii. Vector borne relies greatly on the presence of the secondary host to cause infection. e.g. mosquitos, flies and rats
iv. Droplet organism travels through droplet nuclei that comes out during coughing, sneezing etc.
v. Airborne the organism can uniquely suspend in the air and carried on air current and the like method.
f) Susceptible host any person whose immune defenses are weak or those who are healthy but do not posses adequate specific immunity
ON THE BOARD! Remember that the mode of transmission is the chain that is easiest to break!
THE DEFENSE MECHANISM OF THE BODY The defensive mode is divided into three, namely:
i. 1st line of defense
ii. 2nd line of defense
iii. 3rd line of defense
1st LINE OF DEFENSE Non specific defense mechanism this is the first to come in contact with harmful organism. E.g. skin, saliva,. Tears,
stomach acids, urine etc. 2ND LINE OF DEFENSE Non specific phagocytic response. E.g. phagocytosis by neutrophils.
3RD LINE OF DEFENSE Specific immune response dependent upon the presence of specific anti bodies. E.g. immunity against chickenpox
IMMUNITY Ability of the body to effectively mount an immune response to prevent infection. it is usually dependent on the presence of
antibodies.
a. Natural active contact with infectious organism and the immunity that follows after that.
b. Natural passive immunity received from the mother through the placenta
c. Artificial active immunity gained after the administration of vaccines
d. Artificial passive immunity gained after receiving immune serum or immune globulin.
EPIDEMIOLOGY Refers to study of the pattern and distribution of diseases among the identified population.
a. Endemic the disease is always present in a community the rise and fall remains steadily predictable.
b. Epidemic there is a sharp increase in the number of disease as it affects the population over a period of time and specific locality.
c. Pandemic nations are affected by a disease. It is commonly referred to as international epidemic.
d. Sporadic patches in appearance. The disease does not manifest it self as a dominant entity. Most often the disease affects only a small
portion of the community.
e. Out break the disease has affected the population but the number of the people afflicted is above the endemic proportion but lower than
epidemic levels. An outbreak is an indicator of impending epidemic.
GENERAL MEASURES TO CONTROL COMMUNICABLE DISEASES
Hand washing the most basic of infection control practices. It is the use of soap and water to remove contaminant from our hands.
Disinfection the use of chemicals like alcohol or other physical means to destroy disease causing organism outside the body.
a. Terminal disinfection disinfecting the surroundings of the patient
b. Concurrent disinfection disinfection of substances and materials discharged from the body.
Sterilization all forms of microbial life are eliminated.
Isolation the act of separating an infected patient to prevent cross infection. The following are the types of isolation precaution.
i. First Tier Standard precaution ; applied to all patient regardless of their clinical diagnosis. It is desired that the application of this tie will
protect the nurse and the patient from body fluids including blood as well as wounds or any break in the skin and mucous membrane. Use of
gloves.
ii. Second Tier Transmission based precaution refers to any patient who require more stringent control that necessitates deeper method
than those identified above. These includes contact, airborne and droplet precaution.
a. Contact precaution to protect against direct and indirect transmission. Mask and gown are added.
b. Airborne precaution the use of air filters to prevent infection due to organism suspended in the air.
c. Droplet precaution maintaining a distance of 3 feet from the point source of infection to avoid droplet nuclei. The use of high particulate
mask and goggles are added.
Quarantine the act of limiting the movement and freedom of travel of any patient who have been exposed from an infectious organism.
The length of time is dependent to the maximum incubation period of the suspected disease. Surveillance monitoring of patients, high risk
groups or families to predict, identify and control infection.
CHEMICAL DISINFECTANTS THAT ARE COMMONLY USED
Germicide also known as disinfectant this can kill disease causing organism.
Bactericidal refers to its ability to kill bacteria only.
Bacteriostatic the ability of a chemical agent to halt bacterial reproduction
Antiseptic chemicals that can kill or control the growth of microorganism. This are usually applied on the skin to prevent wound
infection. Soaps and detergents effective against bacteria found in clothes.
Phenols (Lysol) effective against gram negative bacteria.
Alcohol ideally isopropyl alcohol in 70% solution. Effective in killing broad range of microbes.
Chlorine one of the most effective water disinfectants Iodine equally effective with chlorine in antimicrobial activity. This is also used
in skin disinfection (Betadine) Hydrogen Peroxide wound cleanser and disinfectant for surgical devices.
COMMUNICABLE DISEASES NEUROLOGICAL SYSTEM
TETANUS ALSO KNOWN AS LOCK JAW
Description: An acute infection associated with painful muscular spasm
Etiology: Caused by Clostridium tetani which are found on soils and human feces
Mode of transmission: Contamination of wound
Incubation period: 5 10 days
Signs and symptoms
Fever, lock jaw, the most important sign is trismus and risus sardonicus. While
laryngospasm is the most life threatening condition.
Diagnostic procedure
None. History of wound and possible contamination are usually enough to arouse
suspicion and take necessary management.
Management
Wash wound, apply wound antiseptic. Assess for history of immunization Give tetanus
toxoid for negative history of immunization Administer Antitoxin after negative skin
test Penicillin is the drug of choice Prepare for intubation. NGT feeding may become
necessary. Avoid over stimulation to prevent painful muscle contraction. Diazepam is
the drug of choice for muscle spasm
MENINGITIS
Description: An acute inflammation of the meninges
Etiology: Caused by Nesseria meningitides this is usually a normal inhabitant of the nasopharynx.
Mode of transmission: Droplet infection
Incubation period: 2 10 days
Pathophysiology:
The organism enters the bloodstream after invading the respiratory tissues. Reaches the
spinal cord and of course the meninges. It stimulates chemotaxis that leads to leukocyte
infiltration of the meninges. As a result inflammation follows. This build up pressure,
pus and compresses sensitive nervous tissues, that may decrease the level of
consciousness and in more severe cases pus could impede blood flow and brain infarct
my ensue.
Signs and symptoms
The most significant finding indicating meningeal irritation: brudzinski and kernigs
sign. Other sign observable are headache, opisthotonus, fever and petechiae
Diagnostic procedure Lumbar puncture (CSF analysis)
Management
Institute droplet precaution Rifampicin or Ciprofloxacin for prophylaxis Ampicillin is
the drug of choice Ceftriaxone for systemic and CNS infection given in combination
with Ampicillin to combat resistant organism. Mass prophylaxis is not needed provided
that all children in day care centers who have been exposed are exempted hence they
need prophylaxis, this also includes all other children who are close to the infected
patient such as when they share eating utensils. Nurses and Doctors are not at risk of
having the disease except when close contact occurred like in mouth to mouth
resuscitation.
ENCEPHALITIS
Description: Inflammation of the tissues of the Brain
Etiology:
Mosquito borne Japanese enceph, West Nile enceph etc Viral borne Complication
of chicken pox or measles Amebic Acanthamoeba hystolytica
Mode of transmission:
Mosquito borne bite of the infected mosquito Viral may be droplet or airborne
Amebic accidental entry in the naso pharynx due to swimming in infested waters.
Incubation period: Mosquito borne varied Viral 5 15 days Amebic 3 7 days
Pathophysiology:
The infectious organism regardless of the type penetrate the brain and causes
inflammation of the brain tissues it self. the inflammatory response compresses the
brain structure which explains the rapid deterioration of the LOC. Encephalitis is more
severe than meningitis.
Signs and symptoms
Marked decrease in LOC. Brudzinski and kernigs may also be present if meningeal
irritation result. The most significant though is the appearance of decorticate and
decerebate rigidity.
Diagnostic procedure Lumbar Tap (CSF analysis) EEG
Management
Primarily supportive. The body can neutralize the organism thru the presence of
antibody. Amebic encephalitis may benefit from metronidazole. Anti inflammatory may
be given Mannitol could decrease ICP
POLIOMYELITIS
Description: An acute paralytic infection that destroys the affected nerves.
Etiology: Caused by polio virus 1 (Brunhilde), 2 (Lansing), 3 (Leon)
Mode of transmission:
Fecal oral route. Particularly rampant among those in the squatters area who have no
access to sanitary toilet facilities
Incubation period: 7 14 days
Pathophysiology:
The virus enters the oral cavity and reproduces in the intestines which later penetrate
the intestinal wall causing viremia and reaching the motor nerves and the spinal cord.
The virus reproduces inside the nerve and as they are released, the infected cell die,
hence paralysis results.
Signs and symptoms Pokers sign, Haynes sign, tonsillitis, abdominal pain and flaccid paralysis
Diagnostic procedure Stool exam, pandys test, EMG
Management
Prevention OPV No anti viral therapy. Toilet hygiene must be reinforced Watch out for
respiratory paralysis Assist in rehabilitation (physical therapy and comfort measures
OPV is preferred over IPV because the latter can only provide
RABIES
Description: Another acute viral infection which have a zoonotic origin
Etiology: Primarily carried by mammals specially land and aerial mammals. In the Philippines
Dogs and Cats are among the most important reservoir. The causative organism is
Rhabdo Virus
Mode of transmission:
Bite of infected animal. Scratch wound from cats can also cause infection since cats
usually lick their paws.
Incubation period: 10 days for man 14 days for animals
Pathophysiology:
The virus replicates at sight of infection which later proceeds to infect the nearby axons
and then reaches the nerve it self. From that point onwards the virus travels along the
nerve pathway to reach the brain. In the brain the virus insights inflammatory reaction
that give rise to the appearance of encephalitis like symptoms later the organism
descends from the brain and exit to affect other nerves in he body. The affectation of
trigeminal nerve causes throat spasms which gives rise to its classic finding
hydrophobia
Signs and symptoms Hydrophobia, aerophobia, laryngeal, Pharyngeal spasm excessive salivation.
Diagnostic procedure
Fluorescent antibody Staining, Negri bodies found in brain biopsy of the infected
animal
Management
Human Diploid Cell Vaccine, Rabies Immunoglobulin, Rabies Anti serum. tetanus anti
serum is also given if with negative or inadequate immunization history Wash wound
with soap and water, may apply wound antiseptic Once sign and symptoms are present
passive immunization is already useless. Supportive therapy comes next. Protect from
glare and sunlight, protect from water and air current. Cover IV bottle and tubing with
carbon paper or any other else that can effectively hide the iv fluids. Secure consent and
restrain the patient. Observed contact and droplet precaution.
LEPROSY
Description: A chronic infection that usually affects the peripheral nerves and leads to paresthesias
Etiology:
A possible zoonotic infection which is rarely cultured in laboratory but seen to be
growing freely among armadillo. Causative organism is Mycobacterium leprae
Mode of transmission: Droplet infection is the most important transmission. Skin contact may cause infection
only if there is an open lesion with prolonged contact.
Incubation period: 6 months to 8 years
Pathophysiology:
The organism enters the body via droplet infection. It is ingested by macrophages but
cant be killed, as this circulating macrophage reaches the skin the bacteria penetrate
the nerves. Later due to immune recognition WBC attacks the infected cell which
results to the destruction of the affected cell hence the appearance of paresthesias and
consumption of the involved extremity becomes apparent due to immune response it
self.
Signs and symptoms
Painless wound, paresthesias, ulcer that does not heal, leonine appearance, maderosis.
Nerve involvement with acid fast bacilli is the pathognomic sign of leprosy
Diagnostic procedure Scraped incision method.
Management
Institute concurrent disinfection specially of nasal discharge. Prevention is achieved by
BCG immunization Rifampin, Dapsone and lampreme are effective treatment against
this infection
CIRCULATORY SYSTEM
DENGUE HEMORRHAGIC SHOCK SYNDROME
Description: An acute arthropod borne infection which causes massive bleeding.
Etiology:
Causative organism is Dengue virus 1, 2, 3 and 4 the primary vector is Aedes egypti
other wise known as tiger mosquito because of the black stripes present at the dorsal
legs of the insect. The mosquito prefers to thrive on clean stagnant water.
Mode of transmission: Bite of the infected vector mosquito
Incubation period: 6 7 days
Pathophysiology:
The virus is carried by the infected mosquito and transferred through bites in the victim.
Once the proboscis pierced the capillaries it also leaves the viral organism. The virus
mixes in the bloodstream survive and reproduce causing viremia which explains the
appearance of generalized flushing. The virus will then successfully enters the bone
marrow and arrest the maturation of megakaryocyte. Since the precursor of platelets can
not take full course it will result to massive drop in the patients platelet count which
significantly raises the risk for hemorrhage.
Signs and symptoms Petechiae, bleeding, epitaxis, Hermans sign and fever
Diagnostic procedure Tourniquet test, platelet count.
Management
Watch out for bleeding. Minimize injections and other parenteral procedures if possible.
Apply pressure for 10 minutes on injection site. Avoid aspirin use acetaminophen
provide TSB as an adjunct to anti pyretics. Monitor platelet closely. Prepare for platelet
concentrate or fresh whole blood as the need may call for it. Hydrate with PNSS
Preventive measure focuses on 4 o clock habit Use DEET as an effective mosquito
repellant Use mosquito nets
MALARIA
Description: Another type of mosquito borne infection most common in the tropics
Etiology:
The causative organisms are Plasmodium Vivax, Falciparum, Ovale, and Malariae. The
primary vectors are anopheles mosquitoes.
Mode of transmission: Bite of the infected mosquito
Incubation period: For Falciparum 12 days, for Vivax and Ovale 14 days and for Malariae 30 days
Pathophysiology:
From the bite of the infected mosquito the organism enters the body via bloodstream
and immediately proceed to the liver in the form of sporozoites. Inside the hepatocytes
reproduction continues until the host burst releasing the parasite in the form
trophozoites that enters the RBC, inside it the organism divides and form schizont. This
will later produce merozoites that enters RBC the process causes drop in the number of
circulating RBC leading to anemia and cachexia.
Signs and symptoms
A cycle of hot stage (high fever) followed by diaphoretic stage (sweating) and then cold
stage (chilling). The cycle repeats leading to malarial cachexia
Diagnostic procedure Malarial smear or peripheral blood smear
Management
Chloroquine is the drug of choice. Primaquine must be given to prevent relapse. Prevent
by using mosquito repellant and mosquito net Chloroquine is the drug of choice for
prophylaxis.
FILIRIASIS
Description: A chronic lymphatic disorder that is related to elephantiasis
Etiology: Causative organism is Wuchereria bancrofti primary vector Culex spp.
Mode of transmission: Bite of the infected mosquito
Incubation period: 6 12 months
Pathophysiology:
The organism enters the body after the vectors bite, it then matures and migrate on the
lymphatic vessels but it usually affects those in the lower extremity. The protozoal
parasite crowds and destroy the filtering ability of the lymph nodes which then leads to
the accumulation of lymph or body fluids causing edema and at worst cases gross
deformity hence it could lead to elephantiasis.
Signs and symptoms
Recurrent low grade fever, lymphangitis, nocturnal asthma and in worst cases
elephantiasis
Diagnostic procedure Microscopic examination of peripheral blood.
Management
Use of mosquito repellant and nets Hetrazan is effective against Filiriasis adverse
reaction though are seen in a number of patients, if such may be present may use
Ivermectin
RESPIRATORY SYSTEM
DIPHTHERIA
Description:
An acute infection of the upper respiratory system whose complication may include the
lower respiratory tract.
Etiology: The organism, Corynebacterium diphtheriae is ubiquitous.
Mode of transmission: Droplet infection is the means of spread
Incubation period: 1 7 days
Pathophysiology:
The organism infects the oral cavity which later due to its ability of releasing toxins
causes the death of the involved tissues. This gives rise to the appearance of
psudomembarne which may be dislodge and block the airway. As toxins are secreted
the heart, kidney and the nerves absorb it, this toxins halt protein synthesis of the
infected cell which later on causes its death.
Signs and symptoms
Pathognomonic Sign is pseudo membrane. Tonsillitis may also be present. Fever and
malaise. If complication arises paralysis, endocarditis and kidney failure may be seen.
Diagnostic procedure Throat swab
Management
Gather specimen for culture Prepare for epinephrine and possible intubation Be ready
for antitoxin therapy after checking for allergy Administer penicillin or erythromycin
PERTUSIS
Description: A widespread organism that threaten any one who have no immunity against it.
Etiology: Causative organism is Bordetella pertussis
Mode of transmission: Droplet infection
Incubation period: 7 21 days
Pathophysiology:
The organism enters the upper respiratory tract attaches to the respiratory epithelium
and causes an increased production of cyclic amino phosphate that essentially leads to
hyperactivity of the mucous secreting cells. Thick tenacious secretions blocks the
airway. The organism also halts the mucociliary escalator leaving coughing reflex the
last effective protective mechanism of expelling sputum. Due to its relative
tenaciousness the body experiences difficulty in coughing out phlegm thus we observe
patient to manifest violent cough.
Signs and symptoms
Pathognomonic of this infection is violent cough w/out intervening inhalation followed
by an inspiratory whoop. Vomiting may be present, Increased in ICP and IOP are also
seen. Hernia is also a high risk incident.
Diagnostic procedure Throat swab
Management
Penicillin, Erythromycin ; Mucolytic may be ordered. Nebulization may also be
indicated; Provide small feedings Apply abdominal binder ; Avoid dust and drafts
TUBERCULOSIS
Description: A chronic lung infection that leads to consumption of alveolar tissues
Etiology: Causative organism is acid fast bacillus mycobacterium tuberculosis.
Mode of transmission: Droplet infection as well as airborne
Incubation period: 2 4 weeks
Pathophysiology:
The bacilli is inhaled and taken in the alveoli where macrophage will ingest but fail to
kill the organism. As these macrophages migrate to nearby lymph nodes it will die and
leave the capsulated bacteria undigested. Once the bodys immune system dropped, the
bacteria will be activated and stimulate immune response which likewise damage the
alveolar tissues leading to casseation necrosis and could eventually consume the entire
lungs if the process is repeated frequently
Signs and symptoms Afternoon fever, night sweats, cough for 2 weeks, anorexia weight loss.
Diagnostic procedure Sputum microscopy, CXR, Mantoux test
Management
Institute DOTS Give as ordered; Pyrazinamide, Izoniazid, Rifampicin, Ethambutol and
Streptomycin. Check for sensitivity to any of the drug mentioned Provide B6 if
receiving Izoniazid Watch out for visual problem if receiving Ethambutol Ethambutol is
contra indicated for children who cant verbalize visual problems yet.
PNEUMONIA
Description: an acute usually bacterial in nature
Etiology:
the most common causative organism is strptococcus pneumoniae ubiquitous, orgainsm
and may be transferred among population that has poor ventilation and impaired
respiratory cilliary function. certain disease like measles may promote the development
of pneumonia
Mode of transmission: Droplet infection
Incubation period: 24 to 72 hrs usually 48 hrs
Pathophysiology:
the organism enters the respiratory tract and if the cilliary mechanism fails to prevent its
further entry the organism then infects the lower respiratory centers where it stimulate
an inflammatory reaction. this response leads to migration of WBC in particular with
neutrophil hence leukocyte infiltration is seen in chest x-rays as consolidation. the build
up puss increases the alveolar presure causing in atelectasis once collapsed alveoli cant
participate in gas exchange anymore leading to impaired DOB.
Signs and symptoms
Rusty colored sputum is the pathognomonic sign this is caused by WBC infiltrates,
RBC and sputum. DOB, increased RR, coughing and in late cases lethargy, cyanosis
and death.
Diagnostic procedure sputum exam
Management
Co Trimoxazole and gentamycin are the drug of choice. although Co-tri is used more
widely than gentamycin because of its oral preparation which are allowed to be
administered by midwives for patient in far flung areas. instruct the mothers to continue
the administration of antibiotic for 5 straight days TSB if in case fever may arise
Promote proper room ventilation avoid crowding as much as possible Use
Pneumococcal vaccine as indicated
COLDS (CORYZA)
Description: The causative agent comes from adenovirus and rhino virus.
Mode of transmission: Droplet infection, direct contact.
Incubation period: 1 3 days
Pathophysiology:
As the virus enters the respiratory tract, it attaches itself to the mucous membrane and
causes local irritation and inflammation. In response, the mucous membrane releases
mucous to flush out the virus. Since there is an increased in the production of the
mucous it usually flows back and causes rhino rhea and because of the naso-lacrymal
duct, increased mucous production impedes the drainage of tears thus watery eyes is
present. Complications: Children otitis media and bronchopneumonia Adult
sinusitis
Signs and symptoms
General malaise
Fever, chills
Sneezing, dry and scratchy throat
Teary eyes, headache
Continues water discharge from nares
Management
a. Provide adequate rest and sleep b. Increase fluid intake c. Provide adequate and
nutritious diet d. Encourage vitamins specially vitamin C
INFLUENZA (LA GRIPPE OF FLU)
Description: A highly contagious disease characterized by sudden onset of aches and pains.
Etiology: Influenza virus A, B, C
Mode of transmission: Droplet infection, contact with nasopharyngeal secretions
Incubation period: 24 48 hrs.
Pathophysiology:
Upon entry in the upper respiratory tract, it is deposited in the same site and penetrates
the mucosal cells. Causing lysis and destruction of the ciliated epithelium the virus
releases neuramidase that decreases the viscosity of the mucosa. Facilitating the spread
of the infected exudates to the lower respiratory tract, this causes intestinal
inflammation, and necrosis of the alveolar and bronchiolar epithelium. Thus, the alveoli
are filled with exudates containing WBC, RBC and hyaline cartilage. This places the
patient to increased possibility of acquiring bacterial pneumonia usually caused by S.
Aureus.
Signs and symptoms
Respiratory most common
fever
anorexia
chills
muscle pain and aches
coryza
sore throat
bitter taste
orbital pain
Intestinal
vomiting
severe abdominal pain
fever
obstinate constipation
severe diarrhea
Nervous
headache
Management
a. provide adequate rest and ventilation b. tepid sponge bath to reduce the temperature
c. monitor the vital signs d. provide adequate nutrition e. assist the patient in conserving
strength when she is very weak f. drug of choice: antibiotics sulfonamides
INTEGUMENTARY SYSTEM
SCARLET FEVER (SCARLATINA)
Description:
Is an acute, febrile, contagious condition characterized by sudden onset usually with
vomiting and by punctuate erythematous skin eruption followed by characteristic
exfoliation of the skin during convalescence, rapid pulse and sore throat.
Etiology: Group A hemolytic streptococcus group
Mode of transmission: Direct contact, droplet infection and indirect contact
Incubation period: 1 7 days
Pathophysiology:
The bacterium releases erythrogenic toxins, which causes sensitivity reaction in the
body. The toxin can cause toxic injury to the small capillaries of vascular epithelium
found in the body. The skin is the site where the manifestations are most visible where
one will observed strawberry like tongue, rashes, etc. Complications: sinusitis
nephritis otitis media myocarditis/endocarditis mastoiditis
Signs and symptoms
I. Prodomal stage
fever
tachycardia
sore throat
vomiting
headache
abdominal pain
body malaise
II. Eruptive stage
rashes: appears at the end of 24 hours on the chest spread gradually upward and
downward
enanthem: macular eruption on the hard palate
pastias line: due to the grouping of macules found around the folds of the skin
particularly on the elbow
tiny subcuticular vesicles: found in the cuticles of the nails
strawberry tongue: tongue becomes red at the edges and enlarged papillae show
raspberry tongue: circumoral pallor
III. Desquamation (8 10 days) skin begins to peel shedding of the hair and nails
Diagnostic procedure
Scultz-Charlton rash extinction or blanching test for sensitivity to scarlet fever
antitoxin
Dick test determines whether or not a person is naturally immune to scarlatine
nasal swab
Laboratory:
positive throat culture for strep
elevated ASO titer
white and differentiated count high as 50,000 increae in eosinophils
Management

1. isolation medical aseptic technique
2. bed rest
3. keep the patient warm at all times and avoid drafts
4. apply ice cap/packs for high fever
5. give TSB for high temperature
6. increase oral fluid intake
7. take vital signs q 3 4 hrs
8. daily bath should be given: sodium bicarbonate or starch is used in excessive
itching and oil rub after bath is useful
9. use of mouthwashes and gargles for good oral hygiene
10. prevent exoriations by wiping nasal discharges with soft tissues and
application of cold creams
11. encourage daily elimination
12. diet should be of high calorie foods and fruit juices, milk cream and soups
Medical management: a. antitoxins b. convalescent serum c. samma globin
administered IM d. sulfonamides e. antibiotics penicillin (for cleaning the throat of
streptococcus)
LEPROSY (HANSENS DISEASE, HANSENOSIS, LEPRAE, LEONTHIASIS)
Description: A chronic infectious disease characterized by the appearance of modules in the skin or
mucous membranes or by changes in the nerves leading to anesthesia, paralysis or other
changes
Etiology:
Mycobacterium leprae (acid fast bacillus), sporadic/endemic cases, occurs in tropical
and semitropical countries throughout the world. It can be contracted in childhood
(manifested at age 15 and diagnosed by the age of 20 years). Prognosis: > the longer the
time of active disease, severe lesions, the more rapidly they have advanced without
ability to produce the lepromin reaction the poorer the prognosis > case under 21
years old high relapse rate
Mode of transmission: Prolonged intimate skin to skin contact, nasal secretions
Incubation period: Prolonged, undetermined and varies from one to many years
Pathophysiology:
The bacterium, which is an acid-fast bacillus, attacks the skin tissues and peripheral
nerve, which causes skin lesions, anesthesia, infection and deformities
Signs and symptoms
Assessment:
1. Tuberculoid type shows high resistance to Hansens bacilli. Clinical
manifestations are mainly in the skin and nerves and usually are used or non-
infectious.
2. Lepromatous type minimal resistance to the multiplication, existence of the
bacillus, constant presence of large numbers in the lesions and form globi
(characteristic manifestations in the skin and mucus membranes) and peripheral
nerves.
3. Open or infectious cases
4. Inderterminate type clinical manifestations are located chiefly in skin and nerves;
lesions are flat macules.
5. Borderline
Clinical Manifestations: 1. Early stage loss of sensation paralysis of extremities
absence of sweating (anhydrosis) nasal obstruction loss of hair (eyebrows) eye
redness change in the skin color ulcers that does not heal muscle weakness 2. Late
symptoms contractures leonine appearance (due to nodular and thickened skin of the
forehead and face) madarosis (falling of eyebrows) synecomastia sinking of bridge
of nose 3. Cardinal signs presence of Hansens bacilli presence of localized areas of
anesrhesia peripheral nerve enlargement
Diagnostic procedure
1. Lepromin reaction a positive test develops a nodule at the site of inoculation
(first and third week)
2. Wassermann reaction
Management
Planning and implementation
1. Prevention
separate infants from lepromatous parents at birth
segregate and treat open cases of leprosy
require public health supervision and control of cases of Hansens disease
2. Medical management
1. Multiple drug therapy paucibacillary treatment six months or until negative (-)
results occur refampicin once a month dapsone once a day 2. Multibacillary
treatment for 2 consecutive years or until negative (-) for leprosy test rifampicin
once a month lamprene once a day dapsone once a day
1. full, wholesome generous diet
2. alcohol or TSB may be used for high fever
3. patient should have a daily cleansing bath and change of clothing
4. good oral hygiene
5. normal elimination should be maintained
h. meticulous skin care for ulcers
MEASLES (RUBEOLA, MORBILLI, 7 DAY MEASLES)
Description:
An extremely contagious exanthematous disease of acute onset which most often
affects children and the chief symptoms of which are referable to the upper respiratory
passages.
Etiology: The causative agent is the paramyxo virus
Mode of transmission: Nasal throat secretions, droplet infection, indirect contact with articles
Incubation period: 8 20 days
Pathophysiology:
As the virus enters the body it immediately multiplies in the respiratory epiyhelium. It
disseminate by way of the lymphatic system causing hyperplasia of the infected
lymphoid tissue. As a result there is a primary viremia which infects the leukocyte and
involves the whole reticuloendothelial system. As the infected cells die it necrose and
release more viruses to infect other leukocytes leading to secondary viremia, which also
causes edema of upper respiratory tract producing its symptoms and it may predispose
to pneumonia. Complications: otitis media bronchopnuemonia severe bronchitis
Prognosis: death rate is highest in the first two years of life (20%) after 4 years
uncommon over all mortality less than
Signs and symptoms
Assessment:
1. Stages
1. incubation period (average of 10 days) 2. Pre-eruptive stage or stage of invasion (3-6
days) from the appearance of the first signs and symptoms to the earliest evidence of
the eruption. fever, severe cold frequent sneezing profuse nasal discharge eyes are
red and swollen with mucopurulent discharge (lids stick together) Stimsons sign
(puffiness of lower eyelids with definite line of congestion on the conjunctivae)
redness of both eardrums vomiting, drowsiness hard, dry cough Kopliks spot
(appears on second day): small bright, red macules or papules with a tiny or bluish-
white specks on the center and can be found on the buccal cavity macupapular rashes
(seen late in 4th day): appears first on the cheeks or at the hairline true measles rash:
slightly elevated sensation to touch, appears first on the face and spreads downward
over neck, chest trunk, limbs and appearing last on the wrist and back of the hand 3.
Eruptive stage characterized by a general intensification of all local constitutional
symptoms of the pre-eruptive stage with the appearance of bronchitis and loose bowels
irritability and restlessness red and swollen throat enlargement of cervical glands
fever subsides 4. Desquamation stage follows after the rash fades follows the order
of distribution seen in the formation of eruption
Diagnostic procedure No specific diagnostic exam except only for the presence of leucopenia.
Management
a. prevention education of parents regarding the disease passive immunization of
infants and children (gammaglobulin) active immunization (1st year of life) b.
management drugs antibiotics sulfodiazine isolation meticulous skin care
warm alcohol rub to prevent pressure sores good oral and nasal hygiene increase oral
fluid intake proper care of the eyes eye screen to avoid direct light; wear dark
glasses ears should be cleaned after bath if there is discharges patient should lie the
affected ear down or towards the bed
give ample of fluids during febrile stage
GERMAN MEASLES (RUBELLA, ROTHEIN, ROSEOLA, 3-DAY MEASLES)
Description:
An acute infectious disease characterized by mild constitutional symptoms, rose colored
macular eruption which may resembles measles and enlargement and tenderness
Etiology:
Caused by myxovirus. Occurs mostly in spring and seen mostly in children over 5 years
of age
Mode of transmission: Direct contact
Incubation period: 14 21 days Period of communicability 7 days before to 5 days after the rash appears
Pathophysiology:
As the virus gains entrance to the nasopharynx, it immediately invades the nearest
lymph gland causing lymphadenopathy. Later on, the virus enters the blood stream that
stimulates the immune response, which is the cause of rashes found in the body of
infected individual. If rashes has appeared it means that viremia has subsided. Since the
disease is generally mild and serious complication has ha been very rare, what should
be watched out rather are its congenital effects because it can cross the placental barrier,
which may kill the fetus or cause congenital rubella syndrome. Complications: otitis
media encephalitis transient albuminuria arthritis congenital defects for babies
whos mother were exposed in early pregnancy Prognosis: very favorable
Signs and symptoms
fever, cough loss of appetite enlargement of lymph nodes sweating leucopenia
vomiting (in some cases) headache, mild sore throat desquamation follows the rash
enanthem of uvula with tiny red spots rash (cardinal symptom) accompanied with
cervical adenitis: begins on the face including the area around the mouth; oval, pale,
rose-red papules about the size of a pinhead; covers the body within 24 hours and gone
by the end of the 4th day
Management
Planning and implementation a. Prevention: vaccination gamma globulin given to
pregnant women with negative history and who have been exposed in the first trimester
of pregnancy include in MMR given at 15months to the baby b. management
isolation (catarrhal stage to prevent infection to others) bed rest for first few days
meticulous skin care especially after the rash fades good oral and nasal hygiene (use
of petroleum jelly if lips become dry) no special diet is necessary, increase oral fluid
intake
VARICELLA (CHICKEN POX)
Description:
A very contagious acute disease usually occurring in small children, characterized by
the appearance of vesicles frequently preceded by papules, occasionally followed by
postules but ending in crusting
Etiology: Varicella zoster virus (airborne)
Mode of transmission: Droplet infection, direct contact
Incubation period: 2 -3 weeks
Pathophysiology:
The virus gain entrance via the upper respiratory tract it crosses the mucous membrane
and cause systemic infection followed by appearance of numerous macupapular rash.
The rash are fluid filled that contain polymorphonuclear leukocytes. Period of
communicability: highly contagious from 2 days prior to rash to 6 days after rash erupt.
Full blown case imports permanent immunity. Complications: pneumonia nephritis
encephalitis impetigo pitting or scarring of the skin
Signs and symptoms
slight fever: first to appear body malaise, muscle pain eruption (maculopapular)
then progresses to vesicle (3-4 days); begins on trunk and spreads to extremities and
face (even on the scalp, throat and mucus membranes) intense pruritus vesicles
ended as a granular scab irritability
Management 1. Drugs penicillin can be used when the crusts are severe or infected to prevent
scarring or secondary invasion alkalinizing agent to prevent nephritis and to stop
vomiting acyclovir, immunosin antiviral hydrocortisone lotion 1% for itching 2.
isolation in a room by itself 3. provide a well ventilated, warm room to the patient 4.
warm bath should be given daily to relieve itching; use a calamine lotion 5. avoid
injuring the lesions by using soft absorbent towel and the patient should be patted dry
instead of rubbed dry 6. maintain good oral hygiene, if lesions are found in the mouth
or nasal passages, antiseptic prep may be used 7. diet should be regular
HERPES ZOSTER (SHINGLES)
Description:
Acute viral infection of the peripheral nervous system due to reactivation of varicella
zoster virus. The virus causes an inflammatory reaction in isolated spinal and cranial
sensory ganglia and the posterior gray matter of the spinal cord. Contagious to anyone
who has not had varicella or who immunosupressed.
Signs and symptoms
neuralgic pain malaise burning fever cluster of skin vesicles along course of
peripheral sensory nerves (unilateral and found in trunk, thorax or face); appears 3-4
days
Management
1. drugs
analgesics
corticosteroids
acetic acid compresses or white petrolatum
anti-viral (acyclovir)
2. isolate client
3. apply drying lotion
4. administer medications as ordered
5. instruct client to preventive measures
SCABIES
Description:
An infection of the skin produced by burrowing action of a parasite mite resulting in
irritation and the formation of vesicles or postules.
Etiology:
Itchmite, sarcoptes scabei, occurs in individual living in area of poverty where
cleanliness is lacking.
Mode of transmission:
Direct contact with infected persons, indirect contact through soiled bed linens, clothing
and others.
Incubation period: -
Pathophysiology:
Both female and male parasites live on the skin. A female parasite burrows into the
superficial skin to deposit eggs. Pruritus occurs and scratching of skin may produce
secondary infection. Scattered follicular. Eruption contains immature mites.
Inflammation may produce postules and crust. Eggs is hatched in 4 days. Larvae
undergo a series of matts before becoming adult. Life cycle is complete in 1-2 weeks.
Signs and symptoms
intense itching especially at night sites between fingers or flexor surfaces of wrists
and palms, around nipples, umbilicus, in axillary folds, near groin or gluteal folds,
penis, scrotum.
Diagnostic procedure Presence on skin of female mite, ova and feces upon skin scrapping.
Management
1. Take a warm soapy shower bath or bath to remove scaling debris from crusts.
2. Apply prescribed scabicide such as:
lindane lotion (kwell) 1%
crotamiton (Eurax) cream or lotion
6-10% precipitate of sulfur in petrolatum
3. encourage to change clothing frequently
RINGWORM (TRICHOPHYTOSIS)
Description:
A group of diseases caused by a number of vegetable fungi and affecting various
portion of the body in different ways (skin, hair, nails)
Etiology:
TINEA PEDIS (Athletes foot) a superficial fungal infection due to trichophyton
Rubrum, mentagrophytes, or epidermophyton floccosum which may manifest itself as
an acute, inflammatory, vesicular process or as chronic rash involving the soles of the
feet and the inter-digital web spaces. particularly common in summer, contracted
swimming area and locker rooms. TINEA CORPORIS or TINEA CIRCINATA
ringworm of the body. TINEA CRURIS (Jock itch) superficial fungal infection of the
groin which may extend to the inner thigh and buttocks areas and commonly associated
with tinea pedis. TINEA CAPITIS (ringworm of the scalp) caused by microsporum
canis, trichophyton tonsurans. usually spread through child to child contact, use of
towels, combs, brushes and hats kitten and puppies may be the source of the infection
primarily seen in children before puberty
Signs and symptoms
TINEA PEDIS scaly fissures between toes, vesicles on sides of feet pruritus
burning and erethema lymphangitis and cellulites may occur TINEA CORPORIS or
TINEA CIRCINATA intense itching appearance: begins as scaling erythematous
lesions advancing to rings of vesicles with central clearing and appears on exposed
areas of body. TINEA CRURIS dull red brown eruption of the upper thighs and
extends to form circular plaques with elevated scaly or vesicular borders. itching
seen most in joggers, obese individuals and those wearing tight undercoating. TINEA
CAPITIS reddened, oval or round areas of alopecia presence of kerion: an acute
inflammation that produces edema, postules and granulomatous swelling
Diagnostic procedure
TINEA PEDIS direct examination of scrapings (skin, nails, hair) isolation of the
organisms in culture TINEA CAPITIS woods lamp microscopic evaluation
Management
TINEA PEDIS
1. Prevention: instruct client to keep feet dry such as by using talcum powder.
2. Management:
Drugs: topical agent, clotrimazole, miconazole, tolnaftate
Systemic anti-fungal therapy: griseofulvin, ketoconazole
Elevate feet for vesicular type o pain infection.
TINEA CORPORIS or TINEA CIRCINATA
1. Prevention: infected pet is a common source and should be inspected and treated
by a veterinarian.
2. Management
see treatment for tinea pedis
wear clean cotton clothing next to skin
use clean towel daily
dry all areas and skin folds thoroughly
use self monitoring for signs of re-infection after a course of therapy.
TINEA CRURIS
1. Prevention: avoid nylon underclothing, tight-fitting underwear and prolonged
wearing of wet bathing suit.
2. Management:
Drugs topical therapy (miconazole cream); griseofulvin (oral)
avoid excessive washing or scrubbing; wear cotton underwear.
TINEA CAPITIS same with other fungal infection
GASTROINTESTINAL DISORDERS
TYPHOID FEVER (ENTERIC FEVER)
Description:
A general infection characterized by the hyperplasia of the lymphoid tissues, especially
enlargement and ulcerations of the Peyers patches and enlargement of the spleen, by
parechymatous changes in various organs and liberation of an endotoxin in the blood.
Etiology:
Salmonella typhosa, prevalent in temperate climates, high incidence in fall, and mostly
affected are the males and in youth and infant.
Mode of transmission: Infected urine and feces and intake of contaminated food and water
Pathophysiology:
The organism enters the body via the GI tract and invades the walls of the GI tract
leading to bacteremia that localizes in mesenteric lymph nodes, in the masses of
lymphatic tissue, in the mucus membrane of the intestinal wall (Peyers patches) and in
small, solitary lymph follicles in the ileum and colon thus ulceration of the intestines
may result. Complication: perforation of the intestine from erosion of one of the
ulcers intestinal hemorrhage from erosion of blood vessels relapse
thrombophlebitis urinary infection meningitis
Signs and symptoms
1. Gradual onset
severe headache, malaise, muscle pains, non-productive cough
chills and fever, temperature rises slowly
pulse is full and slow
skin eruption irregularly spaced small rose spots on the abdomen, chest and
back; fades 3-4 days
splenomegally
2. Second week
fever remains consistently high abdominal distention and tenderness, constipation or
diarrhea delirium in severe infection coma-vigil look; pupils dilate and patient
appears to stare without seeing sultus tendium twitching of the tendon sets
1. Third week
gradual decline in fever and symptoms subsides
Diagnostic procedure
white blood cell counts blood or bone marrow culture positive urine and stool
cultures in later stage blood serum agglutination (+) at the end of scond week
Management
1. Prevention: decontamination of water sources, milk pasteurization, individual
vaccination of high risk persons, control carriers.
2. Drugs
chloramphenicol
ampicillin
sulfamethoxazole
trimethoprim
furazolidone
3. intravenous infusion to treat dehydration and diarrhea
4. Nursing care

give supportive care
position the patient to prevent aspiration
use of enteric precautions
TSB for high fever
encourage high fluid intake
monitor for complications
1. intestinal decompression procedure, IV fluids and surgical intervention for
perforation
2. withhold food, blood transfusions and bowel resection for intestinal hemorrhage
LEPTOSPIROSIS (WEILS DISEASE, CANICOLA FEVER, HEMMORHAGIC JAUNDICE,
ICTEROHEMORRHAGIC SPIROCHETOSIS, SWINEHERDS DISEASE, MUD FEVER)
Description:
Worldwide in its distribution and especially in areas where sanitation is poorest;
common in Japan. Usually those who are affected are the sewer workers, miners and
swimmers in polluted water.
Etiology: Leptospira icterohaemorrhagiae carried by wild rat
Incubation period: 5 6 days
Signs and symptoms
sudden onset with chills, vomiting and headache by severe fever and pains in the
extremities
intense itching of the conjunctivae
severe jaundice with hemorrhage in the skin and mucus membranes
hematemesis, hematuria and hepatomegaly for severe cases
convalescence occurs in the third week unless there is a complication
Diagnostic procedure Positive agglutination test
Management
Prevention eradication of rats and environmental sanitation Drugs antiserum or
convalescent serum; penicillin Nursing care supportive and symptomatic
DYSENTERY
Etiology:
BACILLARY DYSENTERY (shigellosis, bloody flux) caused by shigella dyseteriae
and shigella paradysenteriae coming from bowel discharges of infected persons and
carriers. VIOLENT DYSENTERY (Cholera) caused by vibrio cholera, vibrio comma
(ogawa and inaba) from infected feces or vomitus.
Mode of transmission:
BACILLARY DYSENTERY eating of contaminated foods, hand to mouth transfer of
contaminated material, flies, objects soiled with discharges of infected person,
contaminated water. VIOLENT DYSENTERY direct or indirect fecal contamination
of water or food supplies by soiled hands, utensils or mechanical carriers such as flies.
Incubation period:
BACILLARY DYSENTERY 1-7 days (average of 4 days) period of
communicability during acute phase and until (-) stool exam VIOLENT
DYSENTERY from a few hours to five days (average 3 days) period of
communicability until the infectious organism is absent from the bowel discharges (7-
14 days)
Signs and symptoms
BACILLARY DYSENTERY chills fever nausea and vomiting tenesmus severe
fiarrhea accompanied by blood and mucus alternating episodes of diarrhea and
constipation (chronic) VIOLENT DYSENTERY
1. Onset
acute colicky pain in the abdomen
mild diarrhea (yellowish)
marked mental depression
headache, vomiting
fever, may or may not be present
2. Collapse stage after 1 or 2 days
profuse watery stools (grayish white or rice water) thirst severe/violent cramps in
the legs and feet thickly furred tongue sunken eyeballs ash-gray colored skin
1. Reaction stage after 3 days
increased consistency of stools skin becomes warm and cyanosis disappear
peripheral circulation improves urine formation increases
Diagnostic procedure
BACILLARY DYSENTERY
stool exam
serologic test
VIOLENT DYSENTERY
(+) stool exam/vomitus
Management
BACILLARY DYSENTERY
1. Methods of control and prevention
recognition of disease and reporting
concurrent disinfection from bowel discharges
investigation of source of infection (food, water and milk supplies, general
sanitation and search for carriers)
prevention of flybreeding, screening
sanitary disposal of human excreta
protection and purification of public water supplies and prevention of
subsequent contamination
2. Drugs
kaolin bismuth and paregoric (combination of sulfonamide) chloramphenicol
1. Nursing care
isolation by medical aseptic technique daily cleansing bath increase oral fluids in
acute stage TSB for fever record and the character of stools passed, amount and
frequency of vomiting VIOLENT DYSENTERY
1. Prevention
immunization screen the sickroom from flies protect the food supplies for
contamination b. Drugs tetracycline c. Replacement of fluids and electrolytes d.
Isolation e. Patient should be spared all unnecessary efforts during the acute stage f.
Buttocks should be kept clean with warm water and soap and rubbed dry g. antiseptic
mouthwash in case of vomiting h. fluids is given as soon as they can be tolerated
MUMPS (INFECTIOUS OR EPIDEMIC PAROTITIS)
Description:
An acute contagious disease the characteristic feature of which is the swelling of one or
both of the parotid glands usually occurring in epidemic form.
Etiology:
Filterable virus, member of myxovirus family, infected oral and nasal secretions is the
source of infection Complication: orchitis or epididymp-orchitis Prognosis: favorable in
most cases of mumps, complete recovery ordinarily takes place even complications take
place.
Mode of transmission:
Direct contact with a person who has the disease or by contact with articles which is
contaminated.
Incubation period:
14 21 days
period of communicability: before the glands is swollen to the time present of
localized swelling
Signs and symptoms
pain in the parotid region
headache
earache
fever
difficulty to open the mouth wide
general malaise
sore throat
Diagnostic procedure
moderate leukocytosis
complement fixation test
skin test for susceptibility to mumps
Management
a. Prevention: immunization (MMR given at 15 months) b. Drugs aspirin for fever,
cortisone c. isolation d. absolute bed rest to prevent complications (at least 4 days) e.
daily bath should be given f. soft bland diet for sore jaw g. advise male to wear well
fitting support to relieve the pull of gravity on the testes and blood vessels h. TSB for
fever i. ice pack/collar application
PARASITISM
Description: -
Etiology:
PINWORM (Enteropiasis) oxyuris vermicularis, occurs from fomites,
autoinfection, fecal contamination, affects one in family and invariably infects entire
family. GIANT INTESTINAL ROUNDWORMS (Ascariasis) ascaris
lumbricoides, from sputum and ova in soil. THREADWORM strongyloides
stercoralis, from fecal soil contamination WHIPWORM (trichuriasis) from fecal
soil contamination HOOKWORM (ancylostomiasis) from larvae in fecal soil
contamination TAPEWORM (taeniasis) Types:
hymenolepis nana from fecal contamination
taenia saginata (beef) from insufficiently cooked meat
taenia solium (pork) contaminated meat
diphyllobothrium latun poorly cooked infested fish
Mode of transmission:
PINWORM mouth GIANT INTESTINAL ROUNDWORMS mouth
THREADWORM enter usually through the skin or feet WHIPWORM mouth
HOOKWORM through skin of the feet TAPEWORM mouth
Signs and symptoms
PINWORM
eosinophilia, itching around the anus, convulsions in children.
GIANT INTESTINAL ROUNDWORMS
chest pain, cough after two months, malnutrition, indigestion, diarrhea, colicky
abdominal pain.
THREADWORM
intermittent diarrhea
WHIPWORM nausea and vomiting, diarrhea, anemia, stunted growth; may cause
prolapse of rectum in children and occasionally appendicitis. HOOKWORM anemia,
diarrhea, stunted growth, bronchial symptoms, obstruction of the biliary and pancreatic
duct.
Diagnostic procedure
PINWORM adults and ova in stool GIANT INTESTINAL ROUNDWORMS adults
and ova in stool THREADWORM larvae WHIPWORM ova in stool
HOOKWORM ova in stool TAPEWORM ova and segments of the worm in the
stool
Management
THREADWORM Prevention: wear shoes and use sanitary toilets
use of sanitary toilets
provide hygiene education of the family
dispose of the infected stools carefully
meticulous cleansing of skin especially anal region, hands and nails
drugs antihelminthic drugs, piperazine citrate, pyrantel pamoate, mebendazole
HEPATITIS
Description:
Widespread inflammation of the liver tissue with liver cell damage due to hepatic cell
degeneration and necrosis; proliferation and enlargement of the Kuffer cells and
inflammation of the periportal areas thus may cause interruption of bile flow.
Etiology:
TYPE A (infectious hepatitis) occurs in crowded living conditions; with poor
personal hygiene or from contaminated food, milk, water or shellfish. Common
occurrence during fall and winter months usually affecting children and young adults.
TYPE B (serum hepatitis, SH virus, viral hepatitis, transfusion hepatitis, homologous
serum jaundice) TYPE C (non-A, non-B hepatitis)
Mode of transmission:
TYPE A fecal/oral route TYPE B blood and body fluids (saliva, semen, vaginal
secretions), often from contaminated needles among IV drug abusers, intimate/sexual
contact. TYPE C by parenteral route, through blood and blood products, needles and
syringes
Incubation period:
TYPE A 15-45 days
period of communicability 3 weeks prior and one week after developing jaundice
TYPE B 50-180 days TYPE C 7-50 days
Pathophysiology: -
Signs and symptoms
a. Pre-icteric stage anorexia nausea and vomiting fatigue constipation or diarrhea
weight loss right upper quadrant discomfort hepatomegaly spleenomegaly
lymphadenopathy b. Icteric stage fatigue weight loss light colored stools dark
urine jaundice pruritus continued hepatomegaly with tenderness c. Post-icteric
stage fatigue but increased sense of well being hepatomegaly: gradually decreasing
Diagnostic procedure
a. All 3 types SGPT, SGOT, alkaline phospatase, bilirubin, ER all increased in pre-
icteric leukocytes, lymphocytes, neutrophils all decreased prolonged PT b. HEPA
A: Hepa A (HAV) in stool before onset Anti-HAV (IgG) appears soon after onset of
jaundice, peaks in 1-2 months and persist indefinitely Anti-HA (IgM) positive in
acute infection lasts 4-6 weeks c. HEPA B HbsAG (surface antigen) positive,
develops 4-12 weeks after infection Anti-HbsAg negative in 80% cases Anti-HBC
associated with infectivity, develops 2-16 weeks after infection ABeAG associated
with ineffectively and disappears before jaundice Anti-Hbe present in carriers,
represents low ineffectivity
Management
a. Prevention I. Type A good hand washing good personal hygiene control and
screening of food handlers passive immunization ISG, to exposed individuals and
prophylaxis for travelers to developing countries II. Type B screen blood donors
HB3Ag use disposable needles and syringes registration of all carriers passive
immunization ISG active immunization hepatavax B vaccine and formalin treated
hepatitis B vaccine given in 3 doses b. Nursing management promote adequate
nutrition small frequent meals of high CHO, moderate to high CHON, high vitamin,
high caloric diet, avoid very hot or cold foods. ensure rest and relaxation
monitor/relive pruritus cool, moist compresses, emollient lotion administer
corticosteroid as ordered isolation procedures as required provide client teaching and
discharge planning with regards to: importance of avoiding alcohol importance of
not donating blood recognition/reporting of signs of inadequate convalescence
avoidance of persons with known infections Drugs liver protector (essentiale,
jectofer, interferon drug)
FOOD POISONING
Description: A gastroenteritis often produced by the presence of a disease organism or its toxins.
Etiology: SALMONELLA GASTROENTERITIS salmonella typhimurium, salmonella
paratyphi A, B, and C; salmonella newport STAPHYLOCOCCUS
GASTROENTERITIS coagulase positive, gram positive: grows rapidly on food
containing carbohydrates Recovery: within 24 36 hours BOTILISM clostridium
botulinum
Incubation period:
SALMONELLA GASTROENTERITIS 6 to 48 hours after the ingestion of
contaminated food STAPHYLOCOCCUS GASTROENTERITIS 2 to 6 hours after
ingestion BOTILISM 24 hours after the ingestion
Signs and symptoms
SALMONELLA GASTROENTERITIS
headache
nausea and vomiting
diarrhea (stools are usually fluid and contain mucus; bloody if in severe infection)
STAPHYLOCOCCUS GASTROENTERITIS
sudden abdominal pain
excessive perspiration
vomiting
diarrhea
pallor weakness
BOTILISM
peripheral nervous system
vomiting ataxia constipation ocular paralysis aphonia other
neufromascular signs
paralysis of the respiratory system which may lead to death
Diagnostic procedure
SALMONELLA GASTROENTERITIS history of illness after ingestion of certain
foods
Management
SALMONELLA GASTROENTERITIS/STAPHYLOCOCCUS GASTROENTERITIS
replacement of fluids and salts
sedatives and anticholinergic to reduce hypermobility of the intestine
good oral hygiene
application of heat to abdomen to relieve cramps
BOTILISM
prevention
regulation of commercial processing of canned foods education of housewives
concerning proper processing of home canned foods canned foods should be boiled
first to destroy the toxins polyvalent antitoxins (botulinum antitoxin)
patient with botulinum should be placed on quiet room and avoidance of
unnecessary activity
symptomatic
intubation for feeding
tracheostomy in respiratory failure
oxygen by IPPB
SEXUALLY TRANSMITTED DISEASE
GONORRHEA (STRAIN, CLAP, JACK, MORNING DROP, G.C. GLEET)
Description:
An infectious disease, which causes inflammation of the mucous membranes of the
genitourinary tract. Complications: MALE bilateral epididymitis, sterility FEMALE
pelvic inflammatory disease, sterility NEWBORN opthalmia neonatorum mother to
child
Etiology: Neisseria gonorrhea
Mode of transmission: Sexual contact
Incubation period: 2 5 days
Signs and symptoms
MALE
burning sensation in the urethra upon urination
passage of purulent (yellowish) discharge
pelvic pain
fever
painful urination
FEMALE
burning sensation upon urination
presence or absence of vaginal discharge
pelvic pain
abdominal distention
nausea and vomiting
urinary frequency
Diagnostic procedure
culture and sensitivity
female: pap smear or cervical smear; male: urethral smear
blood exam VDRL
Management
educate men and women to recognize signs of gonorrhea and to seek immediate
treatment
monitor urinary and vowel elimination
important to treat sexual partner, as client may become re-infected
make arrangements for follow-up culture 2 weeks after therapy is initiated
Drugs penicillin: drug of choice
tetracyclines ceftriaxone sodium (rocephin) amoxicillin (augmentin)
SYPHILIS (LEUS, POX, BAD BLOOD DISEASE)
Description:
A contagious disease that leads to many structural and cutaneous lesions
Complications: a. still birth b. child born with syphilis placenta is bigger than the baby
persistent vesicular eruptions and nasal discharges old man feature mucus patches
on mouth and anus c. child born with late syphilis (signs and symptoms after 2 years)
hutchinsons teeth deafness saddle nose high palate
Etiology: Treponema pallidum
Mode of transmission: Sexual contact
Incubation period: 3 6 weeks
Signs and symptoms
a. Primary syphilis
chancre on genitalia, mouth or anus
serous drainage from chancre
enlarge lymph nodes
maybe painful or painless
highly infectious
b. Secondary syphilis
skin rash on palms and soles of feet
reddish copper colored lesions on palms of hands and soles of feet
condylomas: lesions/sores that fused together
erosions of oral mucus membranes
alopecia
enlarged lymph nodes
fever, headache, sore throat and general malaise
c. Tertiary syphilis
gumma the characteristic lesions
cardiovascular changes
ataxia
stroke, blindness
Diagnostic procedure a. positive test for syphilis venereal disease research laboratory (VDRL) rapid
plasma reagin circle card test (CRPR-CT) automate reagin test (ART) fluorescent
treponemal antibody absorption test (FTA-ABS) wessermann test khan precipitation
test kline, hinton and mazzin tests b. darkfield examination c. culture and sensitivity d.
Management
strict personal hygiene is an absolute requirement
assist in case finding
instruct client to avoid sexual contact until clearance is given by physician
encourage monogamous relationship
explain need to complete course of antibiotic therapy
Drugs penicillin, tetracyclins/kithramycin
ACQUIRED IMMUNE DEFICIENCY SYNDROME (AIDS)
Description: An acquired immune deficiency characterized by a defect in natural immunity
Etiology:
Retrovirus, human immunodeficiency virus (HIV-1 and HIV-2) previously referred to
as human T-lymphotropic virus type III (HTLV-III)
Mode of transmission: Blood transfusion, sexual contact, contaminated needles, perinatal transmission
Incubation period: 6 months to 9 years
Pathophysiology:

Signs and symptoms
anorexia
fatigue
dyspnea
night sweats
fever
diarrhea
enlarged lymph nodes
HIV encephalopathy: memory loss, lack of coordination, partial paralysis, mental
deterioration
HIV wasting syndrome, emaciation
positive test for HIV antibody
positive test for presence of HIV itself
opportunistic infection: neumocystic carinii, cystomegalovirus, kaposis sarcoma
Diagnostic procedure
ELISA test (enzyme-linked immunosorbent assay) a screening test
western blot a confirmatory test
Management
provide frequent rest periods
provide skin care
provide high-calorie, high protein diet to prevent weight loss
provide good oral hygiene
provide oxygen and maintain pulmonary function
provide measures to reduce pain
protect the client from secondary infection; carefully assess for early signs
encourage verbalization of feelings
teach client the importance of:
informing sexual contacts of diagnosis not sharing needle with other individuals
continuing medical supervision
CHLAMYDIAL INFECTION
Description: A sexually transmitted disease that is highly contagious caused by chlamydial organism
Etiology: Chlamydia trachomatis
Mode of transmission: 2 -3 weeks for males
Incubation period: Sexual intercourse
Pathophysiology: -
Signs and symptoms
pruritus in vagina
burning sensation in vagina
painful intercourse
pruritus of urethral meatus in men
burning sensation during urination
Diagnostic procedure Culture of aspirated material from vaginal, anal or penile discharges
Management
doxycycline or azithromycin (recommended for pregnant woman)
universal precaution should be practiced
TRICHOMONIASIS
Description:
Another type of sexually transmitted disease that may also be transmitted by other
means such as handling of infected fomites. It is caused by a protozoan parasites.
Etiology: Trichomonas vaginalis
Mode of transmission: Sexual intercourse, contact with wet towels and wash clothes infected by the organism
Incubation period: 4 20 days, usually 7 days
Signs and symptoms
vaginal discharge
burning and pruritus of vagina
redness of the introitus
usually asymptomatic in men
Diagnostic procedure culture of obtained specimen
Management
metronidazole
sitz bath may relieve symptom
acid douches
tetracyclines may be given on male who are also infected
BIOTERRORISM AND PANDEMICS In the recent course of international conflicts, which has lead to war, has used weapon
that are quite different from the conventional ones used before. The medical science is being used not to prolong life but to
cause immediate death by infection of various biological organisms. The following gives an insight of these dangerous
biological terrorism leading to pandemics.
SMALL POX
Description:
For about two decades the WHO has declared that the world is already small pox
free. Although eliminated in the world over, the specimen is still kept in two
laboratory facility in the United States.
Etiology: Variola virus (DNA virus)
Mode of transmission: Direct contact or by droplet from person to person
Incubation period: 12 days
Signs and symptoms
high fever
malaise
headache
back ache
maculopapular rash in the face, mouth and pharynx (the patients are contagious
after the appearance of the rash)
Management
generally supportive care
before rendering care transmission precaution should be specifically indicated
autoclaving of soiled linens is needed
isolation is necessary until no longer contagious
ANTHRAX
Description:
Also known as whoolsorters disease, the capsulated form of this organism is found in
soil worldwide. The organism needs to take about 8,000 to 50,000 to put a person at
risk of contracting the disease.
Etiology: Bacillus anthracis
Mode of transmission:
inhalation of spores
ingestion of spores
entrance through skin lesions
Incubation period: For inhalation anthrax 60 days, for cutaneous anthrax 1-6 days
Signs and symptoms
a. Inhalation anthrax cough headache fever vomiting chills weakness dyspnea
syncope b. Cutaneous anthrax nausea and vomiting abdominal pain hematochexia
ascites massive diarrhea
Management
a. standard precaution is already sufficient to control the spread of the infection b.
ciprofloxacin/doxycycline is prescribed for mass exposure/casualty with infecting
organism c. important pharmacologic interventions are penicillin, erythromycin,
chlorampenicol and gentamycin
SEVERE ACUTE RESPIRATORY SYNDROME (SARS)
Description:
Latest among all the rest of pandemics which has its origin from China and has spread
to USA, Canada, Philippines and other South East Asian Country
Etiology: Corona virus
Mode of transmission: Airborne
Incubation period: 7 10 days
Signs and symptoms
fever
cough
rapid respiratory compromise
dyspnea
atelectasis
Management supportive treatment
provide ventilatory assistance
use N95 mask to avoid infection