Communicable Disease
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.
Communicable Diseases are Primary Cause of Mortality Gap between Rich and Poor Countries. Non-communicable
diseases account for 59% of all deaths worldwide – estimated to rise from 28m in 1990 to 50m in 2020
About 60% of deaths caused by communicable diseases can be attributed to:
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HIV/AIDS
Malaria
Tuberculosis
Measles
Diarrheal disease
Acute respiratory infection
Goal of WHO
1. Prevention of disease
2. Prevention of disability and death from infection
3.Prevention through immunization
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 doesn’t 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.
1. 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.
2. 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.
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 overall 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
ELEMENTS OF DISEASE CAUSATION (Chain of Infection)
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 or DISEASE
a) Exposure – the stage of contact with the infectious agent
b) Incubation or latent period – the organism successfully entered the body. No apparent illness is present. The
organism is still multiplying to manifest an actual illness. Time interval between the initial infection and the 1st
appearance of any signs and symptoms.
c) Prodromal period – the manifestation of early, vague and mild 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.
1. Period of Illness – overt s/sx of disease, WBC may increase or decrease, can result to death if immune
response or medical intervention fails.
2. Period of Decline – s/sx subside and vulnerable to secondary infection
e) Convalescence Period – the stage of resolution. The body is able to maintain homeostasis. The infectious organism
is under control. Regains strength and the body returns to its pre-diseased state recovery has occurred.
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 for infection to occur.
The following subtopics describe each component of the chain.
1. Pathogen or Causative agent – refers to the biologic agent/ microorganism capable of causing disease such as
fungi, protozoa, parasite, viruses, bacteria etc.
• Eliminate organism by:
o Sterilizing surgical instruments and anything that touches sterile spaces of the body
o Using good food safety methods
o Providing safe drinking water
o Vaccinating people so they do not become reservoirs of illness
o Treating people who are ill
2. Reservoir – Any person, animal, arthropod, plant, soil, or substance (or combination of these) in which an causative
agent normally lives and multiplies, on which it depends primarily for survival, and where it reproduces in such
numbers that it can be transmitted to a susceptible host or simply the medium or body which the microorganism
thrives and survive.
• Eliminate reservoirs by:
o Treating people who are ill
o Vaccinating people
o Handling and disposing of body fluids responsibly
o Handling food safely
o Monitoring soil and contaminated water in sensitive areas of the hospital and washing hands
carefully after contact with either
3. Portal of Entry – hole in the skin that allows the infectious agent to get into the body (mouth, nose, eyes, rashes,
cuts, needlestick injuries, surgical wounds and IV sites)or opening in the body where in the microorganism could
use as passageway to reach the internal physiological structures. For example mouth, nose, wound etc.
• Protect portals of entry (our own and our patients) by:
o Dressings on surgical wounds
o IV site dressings and care
o Elimination of tubes as soon as possible
o Masks, goggles and face shields
o Keeping unwashed hands and objects away from the mouth
o Actions and devices to prevent needlesticks
o Food and water safety
4. Portal of exit – the way the causative agent gets out of the reservoir (body fluid or skin) or any opening to which the
organism uses to exit from the body. Example are anus, nose, vagina, penis, etc.
• Reduce risk from portals of exit by:
o Covering coughs and sneezes with a tissue
o Handling body fluids with gloves, then doing hand hygiene
o Keeping draining wounds covered with a dressing
o Not working when you have exudative (wet) lesions or weeping dermatitis
5. Mode of transmission – any mechanism by which a pathogen is spread from a source or reservoir to a person’s
unwashed hands, things which are not cleaned between patients, droplets, or, for a few diseases, the air or the
method on how the organism travels from one infected host to another. The process of the infectious agent moving
from the reservoir to the susceptible host.
Direct Contact Transmission – requires physical contact from the point source of infection. Such as kissing
and unprotected sexual intercourse.
• Person to person transmission of an agent by
• physical contact between its source and
• susceptible host
• No intermediate object involved
• i.e. kissing, touching, sexual contact
• Source → Susceptible Host
Indirect Contact Transmission – transmitted through fomites and other non-living organism. Contaminated
surgical instruments.
• reservoir to a susceptible host by means of a
• nonliving object (fomites)
• Source → Non Living Object → Susceptible Host
Vector borne – relies greatly on the presence of the secondary host to cause infection. e.g. mosquitos,
flies and rats
• Prevention: Eradicate the source (DOH C.L.E.A.N.)
o C – chemically treated mosquito net
o L – larvae eating fish
o E – environmental sanitation
o A – anti-mosquito
o N – neem tree (oregano, eucalyptus)
• Vector-Borne Diseases
o Dengue Hemorrhagic Fever
o Filariasis
o Leptospirosis
o Malaria
Droplet – organism travels through droplet nuclei that comes out during coughing, sneezing etc.
Airborne – the organism can uniquely suspend in the air and carried on air current and the like method.
i.
ii.
iii.
iv.
v.
•
Eliminate the mode of transmission by:
o Hand hygiene
o Wearing gloves to minimize contamination of hands and discarding them after each patient
o Cleaning, disinfection, or sterilization of equipment used by more than one patient
o Cleaning of the environment, especially high-touch surfaces
6. Susceptible host – a person or animal lacking effective resistance to a particular infectious agent or any person
whose immune defenses are weak or those who are healthy but do not possess adequate specific immunity.
• Recognition of high risk patients
o Immunocompromised
o DM
o Surgery
o Burns
o Elderly
• Minimize risk to susceptible hosts by:
o Vaccinating people against illnesses to which they may be exposed
o Preventing new exposure to infection in people who are already ill, are receiving
immunocompromising treatment, or are infected with HIV
o Maintaining good nutrition
o Maintaining good skin condition
o Covering skin breaks
o Encouraging rest and balance in our lives
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.
Classification of Infectious Disease
1. Based on Behavior within host
a. Infectious Disease – any disease caused by invasion and multiplication of microorganisms
b. Contagious Disease – disease that easily spreads from one person to another
2. Based on Occurrence of Disease
a. Sporadic Disease – disease occurs only occasionally/ patches in appearance. The disease does not manifest
itself as a dominant entity. Most often the disease affects only a small portion of the community.
i.e. botulism, tetanus
b. Endemic Disease – constantly present in a population, country or community. The disease is always present
in a community the rise and fall remains steadily predictable.
i.e. Pulmonary Tuberculosis
c. Epidemic Disease – acquire disease in a relatively short period greater than normal number of cases in an
area within a short period of time. There is a sharp increase in the number of disease as it affects the
population over a period of time and specific locality.
i.e. MERS-COV in Kingdom of Saudi Arabia
d. Pandemic Disease – epidemic disease that occurs worldwide. Nations are affected by a disease. It is
commonly referred to as international epidemic.
i.e. CoViD-19
e. Outbreak – 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.
i.e. Measles Outbreak, Polio Outbreak
3. Based on Severity or Duration of Disease
a. Acute Disease – develops rapidly (rapid onset) but lasts only a short time
i.e. measles, mumps, influenza
b. Chronic Disease – develops slowly, milder but longer lasting clinical manifestation
i.e. Chronic Kidney Disease
4. Based on State of Host Resistance
a. Primary Infection – acute infection that causes the initial illness
b. Secondary Infection – one caused by an opportunistic pathogen after primary infection has weakened the
body’s defenses
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.
c.
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.
d.
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 BY SYSTEM
NERVOUS SYSTEM
TETANUS a.k.a. “LOCK JAW”
Description:
Etiology:
Mode of transmission:
Incubation period:
Signs and symptoms:
Diagnostic procedure:
Management:
An acute infection associated with painful muscular spasm
Caused by Clostridium tetani which are found on soils and human feces
Contamination of wound
5 – 10 days
Fever, lock jaw, the most important sign is trismus and risus sardonicus. While laryngospasm is the most lifethreatening condition.
None. History of wound and possible contamination are usually enough to arouse suspicion and take
necessary 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:
Etiology:
Mode of transmission:
Incubation period:
Pathophysiology:
Signs and symptoms:
An acute inflammation of the meninges
Caused by Neisseria meningitides this is usually a normal inhabitant of the nasopharynx.
Droplet infection
2 – 10 days
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.
The most significant finding indicating meningeal irritation: Brudzinski and Kernig’s sign. Other signs
observable are headache, opisthotonos, fever and petechiae
Diagnostic procedure:
Management:
Lumbar puncture (CSF analysis)
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
Mosquito borne – Japanese encephalitis, West Nile encephalitis, etc.
Etiology:
Viral borne – Complication of chicken pox or measles
Amebic – Acanthamoeba hystolytica
Mosquito borne – bite of the infected mosquito
Mode of transmission: 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
The infectious organism regardless of the type penetrate the brain and causes inflammation of the brain
Pathophysiology:
tissues itself. the inflammatory response compresses the brain structure which explains the rapid
deterioration of the LOC. Encephalitis is more severe than meningitis.
Marked decrease in LOC. Brudzinski and Kernig’s may also be present if meningeal irritation result. The
Signs and symptoms:
most significant though is the appearance of decorticate and decerebrate rigidity.
Diagnostic procedure: Lumbar Tap (CSF analysis) EEG
Primarily supportive. The body can neutralize the organism thru the presence of antibody. Amebic
Management:
encephalitis may benefit from metronidazole. Anti-inflammatory may be given Mannitol could decrease ICP
POLIOMYELITIS
Description:
Etiology:
An acute paralytic infection that destroys the affected nerves.
Caused by polio virus 1 (Brunhilde), 2 (Lansing), 3 (Leon)
Fecal – oral route. Particularly rampant among those in the squatter’s area who have no access to sanitary
Mode of transmission:
toilet facilities
Incubation period:
7 – 14 days
Pathophysiology:
Signs and symptoms:
Diagnostic procedure:
Management:
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 dies, hence paralysis results.
Pokers sign, Haynes sign, tonsillitis, abdominal pain and flaccid paralysis
Stool exam, pandys test, EMG
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
Primarily carried by mammals specially land and aerial mammals. In the Philippines Dogs and Cats are
Etiology:
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
The virus replicates at sight of infection which later proceeds to infect the nearby axons and then reaches the
nerve itself. From that point onwards the virus travels along the nerve pathway to reach the brain. In the
Pathophysiology:
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
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
Management:
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 (also an integumentary problem)
Description:
A chronic infection that usually affects the peripheral nerves and leads to paresthesia
A possible zoonotic infection which is rarely cultured in laboratory but seen to be growing freely among
armadillo. Causative organism is Mycobacterium leprae
Droplet infection is the most important transmission. Skin contact may cause infection only if there is an open
Mode of transmission:
lesion with prolonged contact.
Incubation period:
6 months to 8 years
The organism enters the body via droplet infection. It is ingested by macrophages but can’t be killed, as this
circulating macrophage reaches the skin the bacteria penetrate the nerves. Later due to immune recognition
Pathophysiology:
WBC attacks the infected cell which results to the destruction of the affected cell hence the appearance of
paresthesia and consumption of the involved extremity becomes apparent due to immune response it self.
Painless wound, paresthesia, ulcer that does not heal, leonine appearance, madarosis. Nerve involvement
Signs and symptoms:
with acid fast bacilli is the pathognomonic sign of leprosy
Diagnostic procedure: Scraped incision method.
Institute concurrent disinfection specially of nasal discharge. Prevention is achieved by BCG immunization
Management:
Rifampin, Dapsone and lampreme are effective treatment against this infection
Etiology:
CIRCULATORY SYSTEM
DENGUE HEMORRHAGIC SHOCK SYNDROME/ DENGUE HEMORRHAGIC FEVER
Description:
An acute arthropod borne infection which causes massive bleeding.
Causative organism is Dengue virus (Flaviviridae) 1, 2, 3 and 4 the primary vector is Aedes egypti otherwise
known as tiger mosquito because of the black stripes present at the dorsal legs of the insect. The mosquito
Etiology:
prefers to thrive on clean stagnant water, usually day biting and low flying. Other vectors include: Aedes
albopictus and Culex fatigans.
Mode of transmission: Bite of the infected vector mosquito
Incubation period:
6 – 7 days
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 enter the bone marrow and arrest the maturation of megakaryocyte. Since the precursor of
platelets cannot take full course it will result to massive drop in the patient’s platelet count which significantly
raises the risk for hemorrhage.
Pathophysiology:
Signs/ Symptoms:
Classification of Dengue Fever according to severity
1. Grade I – Dengue fever, saddleback fever plus constitutional signs and symptoms plus positive
tourniquet test
2. Grade II – Stage I plus spontaneous bleeding, epistaxis, GI, cutaneous bleeding
3. Grade III – Dengue Shock Syndrome, all of the following signs and symptoms plus evidence of
circulatory failure
4. Grade IV – Grade III plus irreversible shock and massive bleeding
• First 4 days – Febrile or Invasive stage – high grade fever, headache, body malaise, conjunctival
injection, vomiting, epistaxis or gum bleeding, positive tourniquet test.
• 4th – 7th day – Toxic or Hemorrhagic Stage – After the lyze of the fever, this is where the
complication of dengue is expected to come out as manifested by abdominal pain, melena, indicating
bleeding in the upper gastrointestinal tract, Unstable BP, narrow pulse pressure and shock.
•
Diagnostic procedure:
Management:
7th – 10th day – Convalescent or recovery stage – after 3 days of afebrile stage and the patient was
properly hydrated and monitored BP will become stable and laboratory values of platelet count and
bleeding parameters will begin to normalize.
• Petechiae, bleeding, epistaxis, Herman’s sign and fever
Tourniquet test or Rumpel Leeds Test – presumptive test for capillary fragility
keep cuff inflated for 6-10 mins (child), 10-15 min (adults)
count the petechiae formation 1 sq. inch (>10-15 petechiae/sq. inch)
Laboratory Procedures
CBC
Bleeding Parameters
Serologic test
Dengue blot, Dengue IgM
Other :
PT (Prothrombin Time)
APTT (Activated Partial Thromboplastin Time)
Bleeding time
Coagulation time
Symptomatic and Supportive Management
• Specific Therapy – none
• Symptomatic/Supportive therapy
• Intravenous Fluids (IVF)
• with hemoconcentration, 5-7 ml/kg/hr
• with shock, 10-30ml/kg in <20mins
• Use of Blood/Blood Products
• Platelet concentrate 1 unit/5-7kg
• Cryoprecipitate, 1unit/5kg
• FFP, 15ml/kg x 2-4hrs
• given in patient in impending shock and unresponsive to isotonic or colloid transfusion.
• Prolonged PT
• FWB 20cc/kg
• active bleeding
• check serum calcium
•
PRBC 10cc/kg
Nursing Intervention
• Paracetamol (no aspirin)
• Giving of cytoprotectors
• Gastric Lavage
• trendelenberg position for shock
• Nasal packing with epinephrine
• No intramuscular injections
• manage anxiety of patient and family
Preventive measures
Department of Health program for the control of Dengue Hemorrhagic Fever (4S)
• Seek and destroy breeding places
• S eek early consultation
• Self-protectives clothing e.g. long sleeves, long pants
• Say no to (indiscriminate) left and right defogging
MALARIA
Description:
Another type of mosquito borne infection most common in the tropics
The causative organisms are Plasmodium Vivax, Falciparum, Ovale, and Malariae. The primary vectors are
Etiology:
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
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
Pathophysiology:
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.
A cycle of hot stage (high fever) followed by diaphoretic stage (sweating) and then cold stage (chilling). The
Signs and symptoms:
cycle repeats leading to malarial cachexia
Diagnostic procedure:
Management:
Malarial smear or peripheral blood smear
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
A chronic lymphatic disorder that is related to elephantiasis.
• The disease often progresses to become chronic, debilitating and disfiguring disease since its
Description:
symptoms are unnoticed or unfamiliar to health workers.
• High rates in region 5(bicol), 8 (samar and leyte, II (davao)
Causative organism is Wuchereria bancrofti and Bulgaria malayi. Primary vector: infected female mosquito
Etiology:
(Aedes, Anopheles, Mansonia)
Mode of transmission: Bite of the infected mosquito
Incubation period:
6 – 12 months
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.
Pathophysiology:
Signs and symptoms:
Two biological type
• Nocturnal – microfilaria circulate in peripheral blood at night (10pm – 2am)
• Diurnal – microfilaria circulate in greater concentration at daytime
Acute stage
• filarial fever and lymphatic inflammation that occurs frequently as 10 times per year and usually
abates spontaneously after 7 days
• Lymphadenitis (Inflammation of the lymph nodes)
• Lymphangitis (Inflammation of the lymph vessels)
Chronic Stage (10-15 years from the onset of the first attack)
• Hydrocele (Swelling of the scrotum)
• Lymphedema (Temporary swelling of the upper and lower extremities)
• - Elephantiasis (enlargement and thickening of the skin of the lower or upper extremities)
Other S/Sx
• Recurrent low grade fever, lymphangitis, nocturnal asthma and in worst cases elephantiasis
Diagnostic procedure:
Management:
Microscopic examination of peripheral blood.
• Blood smear – presence of microfilaria
• Immunochromatographic Test (ICT)
• Eosinophil count
• Dietylcarbamazine (DEC) 6mg/KBW in divided doses for 12 consecutive days
• Ivermectin (Mectican)
• Supportive Therapy
• Paracetamol
• Antihistamine for allergic reaction due to DEC
• Vitamin B complex
• Elevation of infected limb, elastic stocking
DEC should be taken immediately after meals
It may cause loss of vision, night blindness, or tunnel vision with prolonged used.
Ivermectin is best taken as single dose with a full glass of water in en empty stomach.
Cannot be used in patient with asthma 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
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
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 pseudomembrane which may be dislodge and block
Signs and symptoms:
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.
Pathognomonic Sign is pseudo membrane. Tonsillitis may also be present. Fever and malaise. If
Diagnostic procedure:
complication arises paralysis, endocarditis and kidney failure may be seen.
Management:
Throat swab
Description:
PERTUSSIS
Description:
Etiology:
Mode of transmission:
Incubation period:
Pathophysiology:
Signs and symptoms:
Diagnostic procedure:
A widespread organism that threaten anyone who have no immunity against it.
Causative organism is Bordetella pertussis
Droplet infection
7 – 21 days
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 block the airway. The organism also halts the muco-ciliary
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.
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.
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:
Etiology:
Mode of transmission:
Incubation period:
Pathophysiology:
Signs and symptoms:
Diagnostic procedure:
Management:
A chronic lung infection that leads to consumption of alveolar tissues
Causative organism is acid fast bacillus mycobacterium tuberculosis.
Droplet infection as well as airborne
2 – 4 weeks
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 body’s immune system dropped, the bacteria will be activated and stimulate immune response
which likewise damage the alveolar tissues leading to cessation, necrosis and could eventually consume the
entire lungs if the process is repeated frequently
Afternoon fever, night sweats, cough for 2 weeks, anorexia weight loss.
Sputum microscopy, CXR, Mantoux test
Institute DOTS Give as ordered; Pyrazinamide, Isoniazid, Rifampicin, Ethambutol and Streptomycin. Check
for sensitivity to any of the drug mentioned Provide B6 if receiving Isoniazid Watch out for visual problem if
receiving Ethambutol. Ethambutol is contra indicated for children who can’t verbalize visual problems yet.
PNEUMONIA
Description:
an acute usually bacterial in nature
the most common causative organism is streptococcus pneumoniae ubiquitous, organism and may be
Etiology:
transferred among population that has poor ventilation and impaired respiratory ciliary 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
the organism enters the respiratory tract and if the ciliary mechanism fails to prevent its further entry the
organism then infects the lower respiratory centers where it stimulates an inflammatory reaction. this
Pathophysiology:
response leads to migration of WBC in particular with neutrophil hence leukocyte infiltration is seen in chest
x-rays as consolidation. the buildup puss increases the alveolar pressure causing in atelectasis once
collapsed alveoli cant participate in gas exchange anymore leading to impaired DOB.
Signs and symptoms:
Diagnostic procedure:
Management:
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.
sputum exam
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:
Etiology:
Mode of transmission:
Incubation period:
Pathophysiology:
Signs and symptoms:
Diagnostic procedure:
Management:
Runny nose
The causative agent comes from adenovirus and rhino virus.
Droplet infection, direct contact.
1 – 3 days
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-lachrymal duct, increased mucous production impedes the drainage of tears thus watery eyes is
present. Complications: Children – otitis media and bronchopneumonia Adult – sinusitis
• General malaise
• Fever, chills
• Sneezing, dry and scratchy throat
• Teary eyes, headache
Continues water discharge from nares
a. Provide adequate rest and sleep
b. Increase fluid intake
c. Provide adequate and nutritious diet
d. Encourage vitamins specially vitamin C
Droplet infection, direct contact.
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.
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
Pathophysiology:
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.
Respiratory – most common
• fever
• anorexia
• chills
• muscle pain and aches
• coryza
• sore throat
• bitter taste
Signs and symptoms:
• orbital pain
Intestinal
• vomiting
• severe abdominal pain
• fever
• obstinate constipation
• severe diarrhea
Nervous
headache
a. provides adequate rest and ventilation
b. tepid sponge bath to reduce the temperature
c. monitors the vital signs
Management:
d. provides adequate nutrition
e. assists the patient in conserving strength when she is very weak
f. drug of choice: · antibiotics · sulfonamides
INTEGUMENTARY SYSTEM
SCARLET FEVER (SCARLATINA)
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
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
Signs and symptoms:
the manifestations are most visible where one will observe strawberry like tongue, rashes, etc.
Complications: · sinusitis · nephritis · otitis media · myocarditis/endocarditis · mastoiditis
I. Prodromal stage
• fever
• tachycardia
• sore throat
• vomiting
• headache
• abdominal pain
• body malaise
Diagnostic procedure: 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
• pastia’s 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
Management:
Description:
Schultz-Charlton rash extinction or blanching test – for sensitivity to scarlet fever antitoxin
Dick test – determines whether or not a person is naturally immune to scarlatina
nasal swab
Laboratory:
• positive throat culture for strep
• elevated ASO titer
white and differentiated count high as 50,000 increase in eosinophils
•
•
•
LEPROSY (HANSEN’S DISEASE, HANSENOSIS, LEPRAE, LEONTHIASIS)
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
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
Etiology:
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
The bacterium, which is an acid-fast bacillus, attacks the skin tissues and peripheral nerve, which causes
Pathophysiology:
skin lesions, anesthesia, infection and deformities
Assessment:
1. Tuberculoid type – shows high resistance to Hansen’s 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
Signs and symptoms:
mucus membranes) and peripheral nerves.
3. Open or infectious cases
4. Indeterminate type – clinical manifestations are located chiefly in skin and nerves; lesions are flat
macules.
5. Borderline
Clinical Manifestations:
Description:
Diagnostic procedure:
Management:
1. Early stage · loss of sensation · paralysis of extremities · absence of sweating (anhidrosis) · 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) · gynecomastia · sinking of bridge of nose
3. Cardinal signs · presence of Hansen’s bacilli · presence of localized areas of anesrhesia · peripheral
nerve enlargement
1. Lepromin reaction – a positive test develops a nodule at the site of inoculation (first and third week)
Wassermann reaction
Planning and implementation
1. Prevention
o separate infants from lepromatous parents at birth
o segregate and treat open cases of leprosy
o require public health supervision and control of cases of Hansen’s disease
2. Medical management
1. Multiple drug therapy · paucibacillary treatment – six months or until negative (-) results occur ·
rifampicin – once a month · dapsone - once a day
2. Multibacillary treatment – for 2 consecutive years or until negative (-) for leprosy test · rifampicin
once a month · lampreme once a day · dapsone once a day
3. full, wholesome generous diet
4. alcohol or TSB may be used for high fever
5. patient should have a daily cleansing bath and change of clothing
6. good oral hygiene
7. normal elimination should be maintained
8. meticulous skin care for ulcers
MEASLES (RUBEOLA, MORBILLI, 7 – DAY MEASLES)
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
Description:
Pathophysiology:
Signs and symptoms:
As the virus enters the body it immediately multiplies in the respiratory epithelium. It disseminates 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 · bronchopneumonia · severe bronchitis Prognosis: · death rate is highest in the
first two years of life (20%) · after 4 years – uncommon · over all mortality – less than
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) · Stimson’s
sign (puffiness of lower eyelids with definite line of congestion on the conjunctivae) · redness of both
eardrums · vomiting, drowsiness · hard, dry cough · Koplik’s 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 · maculo-papular 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
Diagnostic procedure:
4. Desquamation stage · follows after the rash fades · follows the order of distribution seen in the
formation of eruption
No specific diagnostic exam except only for the presence of leucopenia.
a. prevention · education of parents regarding the disease · passive immunization of infants and children
(gamma globulin) · active immunization (1st year of life)
Management:
b. management · drugs Ø antibiotics Ø sulfadiazine · 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)
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
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 have appeared it means that viremia
has subsided. Since the disease is generally mild and serious complication has ha been very rare, what
Pathophysiology:
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 whose mother were exposed in early pregnancy
Prognosis: very favorable
· 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 ·
Signs and symptoms: 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
Planning and implementation
Description:
Management:
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)
A very contagious acute disease usually occurring in small children, characterized by the appearance of
vesicles frequently preceded by papules, occasionally followed by pustules but ending in crusting
Etiology:
Varicella zoster virus (airborne)
Mode of transmission: Droplet infection, direct contact
Incubation period:
2 -3 weeks
The virus gain entrance via the upper respiratory tract it crosses the mucous membrane and cause systemic
infection followed by appearance of numerous maculopapular rash. The rash are fluid filled that contain
Pathophysiology:
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
· slight fever: first to appear · body malaise, muscle pain · eruption (maculopapular) then progresses to
Signs and symptoms: 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
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
Management:
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
Description:
HERPES ZOSTER (SHINGLES)
Description:
Signs and symptoms:
Management:
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 immunosuppressed.
· 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
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
instruct client to preventive measures
o
o
o
o
SCABIES
An infection of the skin produced by burrowing action of a parasite mite resulting in irritation and the
formation of vesicles or pustules.
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:
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
Pathophysiology:
contains immature mites. Inflammation may produce pustules 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.
· intense itching especially at night · sites – between fingers or flexor surfaces of wrists and palms,
Signs and symptoms:
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.
1. Take a warm soapy shower bath or bath to remove scaling debris from crusts.
2. Apply prescribed scabicide such as:
o lindane lotion (kwell) 1%
Management:
o crotamiton (Eurax) cream or lotion
o 6-10% precipitate of sulfur in petrolatum
3. encourage to change clothing frequently
Description:
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)
TINEA PEDIS (Athlete’s 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.
Etiology:
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 ·
TINEA PEDIS · scaly fissures between toes, vesicles on sides of feet · pruritus · burning and erythema ·
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.
Signs and symptoms:
Diagnostic procedure:
Management:
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, pustules and granulomatous swelling
TINEA PEDIS · direct examination of scrapings (skin, nails, hair) · isolation of the organisms in culture
TINEA CAPITIS · wood’s lamp · microscopic evaluation
TINEA PEDIS
1. Prevention: instruct client to keep feet dry such as by using talcum powder.
2. Management:
o Drugs: topical agent, clotrimazole, miconazole, tolnaftate
o Systemic anti-fungal therapy: griseofulvin, ketoconazole
o 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
o see treatment for tinea pedis
o wear clean cotton clothing next to skin
o use clean towel daily
o dry all areas and skin folds thoroughly
o 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:
o Drugs – topical therapy (miconazole cream); griseofulvin (oral)
o avoid excessive washing or scrubbing; wear cotton underwear.
TINEA CAPITIS – same with other fungal infection
CIRCULATORY SYSTEM
MENINGITIS
A general infection characterized by the hyperplasia of the lymphoid tissues, especially enlargement and
ulcerations of the Peyer’s patches and enlargement of the spleen, by parenchymatous changes in various
organs and liberation of an endotoxin in the blood.
Salmonella typhosa, prevalent in temperate climates, high incidence in fall, and mostly affected are the males
Etiology:
and in youth and infant.
Mode of transmission: Infected urine and feces and intake of contaminated food and water
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 (Peyer’s patches) and in small, solitary lymph follicles in the ileum and colon thus ulceration of
Pathophysiology:
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
1. Gradual onset
o severe headache, malaise, muscle pains, non-productive cough
o chills and fever, temperature rises slowly
o pulse is full and slow
o skin eruption – irregularly spaced small rose spots on the abdomen, chest and back; fades 3-4
days
Signs and symptoms:
o splenomegaly
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
3. Third week
· gradual decline in fever and symptoms subsides
· white blood cell counts · blood or bone marrow culture · positive urine and stool cultures in later stage · blood
Diagnostic procedure:
serum agglutination – (+) at the end of second week
Description:
Management:
1. Prevention: decontamination of water sources, milk pasteurization, individual vaccination of high risk
persons, control carriers.
2. Drugs
o chloramphenicol
o ampicillin
o sulfamethoxazole
o trimethoprim
o furazolidone
3. intravenous infusion – to treat dehydration and diarrhea
4. Nursing care
o give supportive care
o position the patient to prevent aspiration
o use of enteric precautions
o TSB for high fever
o encourage high fluid intake
o monitor for complications
5. intestinal decompression procedure, IV fluids and surgical intervention – for perforation
withhold food, blood transfusions and bowel resection – for intestinal hemorrhage
LEPTOSPIROSIS (WEIL’S DISEASE, CANICOLA FEVER, HEMMORHAGIC JAUNDICE, ICTEROHEMORRHAGIC
SPIROCHETOSIS, SWINEHERD’S DISEASE, MUD FEVER)
Description:
Etiology:
Incubation period:
Signs and symptoms:
Diagnostic procedure:
Management:
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.
Leptospira ictero-haemorrhagiae carried by wild rat
5 – 6 days
• 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
Positive agglutination test
Prevention – eradication of rats and environmental sanitation Drugs – antiserum or convalescent serum;
penicillin Nursing care – supportive and symptomatic
DYSENTERY
BACILLARY DYSENTERY (shigellosis, bloody flux) – caused by shigella dysenteriae 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.
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
Mode of transmission:
or indirect fecal contamination of water or food supplies by soiled hands, utensils or mechanical carriers such
as flies.
BACILLARY DYSENTERY – 1-7 days (average of 4 days) · period of communicability – during acute phase
Incubation period:
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) ·
BACILLARY DYSENTERY · chills · fever · nausea and vomiting · tenesmus · severe diarrhea accompanied
by blood and mucus · alternating episodes of diarrhea and constipation (chronic) VIOLENT DYSENTERY
1. Onset
o acute colicky pain in the abdomen
o mild diarrhea (yellowish)
o marked mental depression
o headache, vomiting
Signs and symptoms:
o 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
3. Reaction stage – after 3 days
· increased consistency of stools · skin becomes warm and cyanosis disappear · peripheral circulation
improves · urine formation increases
BACILLARY DYSENTERY
• stool exam
Diagnostic procedure:
• serologic test
VIOLENT DYSENTERY
(+) stool exam/vomitus
BACILLARY DYSENTERY
Management:
1. Methods of control and prevention
Etiology:
o
o
o
o
o
o
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 fly breeding, 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
3. 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)
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.
Filterable virus, member of myxovirus family, infected oral and nasal secretions is the source of infection
Etiology:
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.
14 – 21 days
Incubation period:
period of communicability: before the glands is swollen to the time present of localized swelling
• pain in the parotid region
• headache
• earache
Signs and symptoms:
• fever
• difficulty to open the mouth wide
• general malaise
Description:
Diagnostic procedure:
Management:
•
•
•
sore throat
moderate leukocytosis
complement fixation test
skin test for susceptibility to mumps
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:
· 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
Etiology:
(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
PINWORM – mouth GIANT INTESTINAL ROUNDWORMS – mouth THREADWORM – enter usually through
Mode of transmission:
the skin or feet WHIPWORM – mouth HOOKWORM – through skin of the feet TAPEWORM - mouth
PINWORM
• eosinophilia, itching around the anus, convulsions in children.
GIANT INTESTINAL ROUNDWORMS
• chest pain, cough after two months, malnutrition, indigestion, diarrhea, colicky abdominal pain.
Signs and symptoms: 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:
Management:
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
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 – anthelminthic drugs, piperazine citrate, pyrantel pamoate, mebendazole
HEPATITIS
Widespread inflammation of the liver tissue with liver cell damage due to hepatic cell degeneration and
necrosis; proliferation and enlargement of the Kupffer cells and inflammation of the periportal areas thus may
cause interruption of bile flow.
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
Etiology:
children and young adults. TYPE B (serum hepatitis, SH virus, viral hepatitis, transfusion hepatitis, homologous
serum jaundice) TYPE C (non-A, non-B hepatitis)
TYPE A – fecal/oral route TYPE B – blood and body fluids (saliva, semen, vaginal secretions), often from
Mode of transmission: contaminated needles among IV drug abusers, intimate/sexual contact. TYPE C – by parenteral route, through
blood and blood products, needles and syringes
TYPE A – 15-45 days
Incubation period:
• period of communicability – 3 weeks prior and one week after developing jaundice
TYPE B – 50-180 days TYPE C – 7-50 days
Pathophysiology:
a. Pre-icteric stage · anorexia · nausea and vomiting · fatigue · constipation or diarrhea · weight loss · right
upper quadrant discomfort · hepatomegaly · splenomegaly · lymphadenopathy b. Icteric stage · fatigue · weight
Signs and symptoms:
loss · light colored stools · dark urine · jaundice · pruritus · continued hepatomegaly with tenderness c. Posticteric stage · fatigue but increased sense of wellbeing · hepatomegaly: gradually decreasing
a. All 3 types · SGPT, SGOT, alkaline phosphatase, bilirubin, ER – all increased in pre-icteric · leukocytes,
Diagnostic procedure: 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
Description:
Management:
(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
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: Ø
importance of avoiding alcohol Ø importance of not donating blood Ø recognition/reporting of signs of
inadequate convalescence Ø avoidance of persons with known infections · Drugs – liver protector (essentiale,
jectofer, interferon drug)
FOOD POISONING
Description:
Etiology:
Incubation period:
Signs and symptoms:
A gastroenteritis often produced by the presence of a disease organism or its toxins.
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
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
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
•
Diagnostic procedure:
Management:
pallor weakness
BOTILISM
• peripheral nervous system
Ø vomiting Ø ataxia Ø constipation Ø ocular paralysis Ø aphonia Ø other neufromascular signs
paralysis of the respiratory system which may lead to death
SALMONELLA GASTROENTERITIS – history of illness after ingestion of certain foods
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
Ø regulation of commercial processing of canned foods Ø education of housewives concerning proper
processing of home canned foods Ø canned foods should be boiled first to destroy the toxins Ø 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 INFECTIONS/ DISEASES
GONORRHEA (STRAIN, CLAP, JACK, MORNING DROP, G.C. GLEET)
An infectious disease, which causes inflammation of the mucous membranes of the genitourinary tract.
Description:
Complications: MALE – bilateral epididymitis, sterility FEMALE – pelvic inflammatory disease, sterility
NEWBORN – ophthalmia neonatorum – mother to child
Etiology:
Neisseria gonorrhea
Mode of transmission: Sexual contact
Incubation period:
2 – 5 days
MALE
• burning sensation in the urethra upon urination
• passage of purulent (yellowish) discharge
• pelvic pain
• fever
• painful urination
Signs and symptoms: 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
Ø tetracyclines Ø ceftriaxone sodium (rocephin) Ø amoxicillin (augmentin)
SYPHILIS (LEUS, POX, BAD BLOOD DISEASE)
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
Description:
man feature · mucus patches on mouth and anus c. child born with late syphilis (signs and symptoms after 2
years) · Hutchinson’s teeth · deafness · saddle nose · high palate
Etiology:
Treponema pallidum
Mode of transmission: Sexual contact
Incubation period:
3 – 6 weeks
a. Primary syphilis
• chancre on genitalia, mouth or anus
• serous drainage from chancre
• enlarge lymph nodes
• maybe painful or painless
• highly infectious
Signs and symptoms: 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
•
Diagnostic procedure:
Management:
fever, headache, sore throat and general malaise
c. Tertiary syphilis
• gumma – the characteristic lesions
• cardiovascular changes
• ataxia
stroke, blindness
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.
•
•
•
•
•
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
Retrovirus, human immunodeficiency virus (HIV-1 and HIV-2) previously referred to as human T-lymphotropic
Etiology:
virus type III (HTLV-III)
Mode of transmission: Blood transfusion, sexual contact, contaminated needles, perinatal transmission
Incubation period:
6 months to 9 years
Pathophysiology:
• anorexia
• fatigue
• dyspnea
Signs and symptoms:
• night sweats
• fever
• diarrhea
• enlarged lymph nodes
•
•
•
•
Diagnostic procedure:
Management:
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: pneumocystis carinii, cytomegalovirus, Kaposi’s sarcoma
• ELISA test (enzyme-linked immunosorbent assay) – a screening test
western blot – a confirmatory test
• 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:
Ø informing sexual contacts of diagnosis Ø not sharing needle with other individuals Ø continuing medical
supervision
CHLAMYDIAL INFECTION
Description:
Etiology:
Mode of transmission:
Incubation period:
Pathophysiology:
Signs and symptoms:
Diagnostic procedure:
Management:
A sexually transmitted disease that is highly contagious caused by chlamydial organism
Chlamydia trachomatis
2 -3 weeks for males
Sexual intercourse
• pruritus in vagina
• burning sensation in vagina
• painful intercourse
• pruritus of urethral meatus in men
burning sensation during urination
Culture of aspirated material from vaginal, anal or penile discharges
• doxycycline or azithromycin (recommended for pregnant woman)
universal precaution should be practiced
TRICHOMONIASIS
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
Description:
Signs and symptoms:
Diagnostic procedure:
Management:
•
•
•
vaginal discharge
burning and pruritus of vagina
redness of the introitus
usually asymptomatic in men
culture of obtained specimen
•
•
•
metronidazole
sitz bath may relieve symptom
acid douches
tetracyclines may be given on male who are also infected
BIOTERRORISM AND PANDEMICS
SMALLPOX
For about two decades the WHO has declared that the world is already “smallpox 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
• high fever
• malaise
• headache
Signs and symptoms:
• back ache
maculopapular rash in the face, mouth and pharynx (the patients are contagious after the appearance of the
rash)
• generally supportive care
• before rendering care transmission precaution should be specifically indicated
Management:
• autoclaving of soiled linens is needed
isolation is necessary until no longer contagious
Description:
ANTHRAX
Description:
Etiology:
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.
Bacillus anthracis
•
•
inhalation of spores
Mode of transmission:
ingestion of spores
entrance through skin lesions
Incubation period:
For inhalation anthrax 60 days, for cutaneous anthrax 1-6 days
a. Inhalation anthrax · cough · headache · fever · vomiting · chills · weakness · dyspnea · syncope
Signs and symptoms:
b. Cutaneous anthrax · nausea and vomiting · abdominal pain · hematochezia · ascites · massive diarrhea
a. standard precaution is already sufficient to control the spread of the infection
Management:
b. ciprofloxacin/doxycycline is prescribed for mass exposure/casualty with infecting organism c. important
pharmacologic interventions are penicillin, erythromycin, chloramphenicol and gentamycin
SEVERE ACUTE RESPIRATORY SYNDROME (SARS)
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
• fever
• cough
Signs and symptoms:
• rapid respiratory compromise
• dyspnea
atelectasis
• supportive treatment
Management:
• provide ventilatory assistance
use N95 mask to avoid infection
Description:
CoViD-19 (CORONAVIRUS DISEASE/ SARS-COV2/ NCoV)
COVID-19 is the disease caused by a new coronavirus called SARS-CoV-2. WHO first learned of this new
virus on 31 December 2019, following a report of a cluster of cases of ‘viral pneumonia’ in Wuhan, People’s
Republic of China.
Etiology:
Corona Virus
Mode of transmission: Droplet and Airborne
Incubation period:
3-7 days
Description:
The most common symptoms of COVID-19 are
• Fever
•
•
Dry cough
Fatigue
Other symptoms that are less common and may affect some patients include:
• Loss of taste or smell,
Signs and symptoms:
•
•
•
•
•
•
•
•
•
Nasal congestion,
Conjunctivitis (also known as red eyes)
Sore throat,
Headache,
Muscle or joint pain,
Different types of skin rash,
Nausea or vomiting,
Diarrhea,
Chills or dizziness.
Symptoms of severe COVID‐19 disease include:
• Shortness of breath,
•
•
•
•
Loss of appetite,
Confusion,
Persistent pain or pressure in the chest,
High temperature (above 38 °C).
Other less common symptoms are:
• Irritability,
•
•
•
•
•
•
Confusion,
Reduced consciousness (sometimes associated with seizures),
Anxiety,
Depression,
Sleep disorders,
More severe and rare neurological complications such as strokes, brain inflammation, delirium and
nerve damage.
People of all ages who experience fever and/or cough associated with difficulty breathing or shortness of
breath, chest pain or pressure, or loss of speech or movement should seek medical care immediately. If
possible, call your health care provider, hotline or health facility first, so you can be directed to the right clinic.
•
in most situations, a molecular test is used to detect SARS-CoV-2 and confirm infection. Polymerase
chain reaction (PCR) is the most commonly used molecular test. Samples are collected from the nose
and/or throat with a swab. Molecular tests detect virus in the sample by amplifying viral genetic material
to detectable levels. For this reason, a molecular test is used to confirm an active infection, usually within
a few days of exposure and around the time that symptoms may begin.
•
Rapid antigen tests (sometimes known as a rapid diagnostic test – RDT) detect viral proteins (known as
antigens). Samples are collected from the nose and/or throat with a swab. These tests are cheaper than
PCR and will offer results more quickly, although they are generally less accurate. These tests perform
best when there is more virus circulating in the community and when sampled from an individual during
the time they are most infectious.
•
Scientists around the world are working to find and develop treatments for COVID-19.
•
Optimal supportive care includes oxygen for severely ill patients and those who are at risk for severe
disease and more advanced respiratory support such as ventilation for patients who are critically ill.
Dexamethasone is a corticosteroid that can help reduce the length of time on a ventilator and save lives
of patients with severe and critical illness. Read our dexamethasone Q&A for more information.
Results from the WHO’s Solidarity Trial indicated that remdesivir, hydroxychloroquine,
lopinavir/ritonavir and interferon regimens appear to have little or no effect on 28-day mortality or the
in-hospital course of COVID-19 among hospitalized patients.
•
Management:
•
•
Hydroxychloroquine has not been shown to offer any benefit for treatment of COVID-19. Read
our hydroxychloroquine Q&A for more information.
•
•
•
WHO does not recommend self-medication with any medicines, including antibiotics, as a prevention
or cure for COVID-19. WHO is coordinating efforts to develop treatments for COVID-19 and will continue
to provide new information as it becomes available.
Antibiotics do not work against viruses; they only work on bacterial infections. COVID-19 is caused by
a virus, so antibiotics do not work. Antibiotics should not be used as a means of prevention or treatment
of COVID-19.
In hospitals, physicians will sometimes use antibiotics to prevent or treat secondary bacterial infections
which can be a complication of COVID-19 in severely ill patients. They should only be used as directed
by a physician to treat a bacterial infection.