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 like wise the focus of community health nursing.
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 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. 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|
|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.|
|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|
|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|
|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.|
|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 can’t 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|
|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 patient’s platelet count which significantly raises the risk for hemorrhage.|
|Signs and symptoms||Petechiae, bleeding, epitaxis, Herman’s 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|
|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.|
|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|
|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|
|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|
|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 body’s 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.|
|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|
|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||
|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
|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|
|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
II. Eruptive stage
III. Desquamation (8 – 10 days) · skin begins to peel · shedding of the hair and nails
Medical management: a. antitoxins b. convalescent serum c. samma globin – administered IM d. sulfonamides e. antibiotics – penicillin (for cleaning the throat of streptococcus)
|LEPROSY (HANSEN’S 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:
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 Hansen’s bacilli · presence of localized areas of anesrhesia · peripheral nerve enlargement
|Management||Planning and implementation
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
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. 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 · 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 Ø antibiotics Ø 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 who’s 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|
|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.|
|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.|
|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 (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. 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 · wood’s lamp · microscopic evaluation|
TINEA CORPORIS or TINEA CIRCINATA
TINEA CAPITIS – same with other fungal infection
|TYPHOID FEVER (ENTERIC FEVER)|
|Description:||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 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 (Peyer’s 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||
· 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
· 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|
|LEPTOSPIROSIS (WEIL’S DISEASE, CANICOLA FEVER, HEMMORHAGIC JAUNDICE, ICTEROHEMORRHAGIC SPIROCHETOSIS, SWINEHERD’S 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||
|Diagnostic procedure||Positive agglutination test|
|Management||Prevention – eradication of rats and environmental sanitation Drugs – antiserum or convalescent serum; penicillin Nursing care – supportive and symptomatic|
|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
· 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
· increased consistency of stools · skin becomes warm and cyanosis disappear · peripheral circulation improves · urine formation increases
|Diagnostic procedure||BACILLARY DYSENTERY
· kaolin · bismuth and paregoric (combination of sulfonamide) · chloramphenicol
· 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
· 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
|Signs and symptoms||
|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|
|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:
|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
GIANT INTESTINAL ROUNDWORMS
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
|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
TYPE B – 50-180 days TYPE C – 7-50 days
|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: 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)|
|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
Ø vomiting Ø ataxia Ø constipation Ø ocular paralysis Ø aphonia Ø other neufromascular signs
|Diagnostic procedure||SALMONELLA GASTROENTERITIS – history of illness after ingestion of certain foods|
|Management||SALMONELLA GASTROENTERITIS/STAPHYLOCOCCUS GASTROENTERITIS
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)
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|
|Mode of transmission:||Sexual contact|
|Incubation period:||2 – 5 days|
|Signs and symptoms||MALE
Ø tetracyclines Ø ceftriaxone sodium (rocephin) Ø 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) · hutchinson’s teeth · deafness · saddle nose · high palate|
|Mode of transmission:||Sexual contact|
|Incubation period:||3 – 6 weeks|
|Signs and symptoms||a. Primary syphilis
b. Secondary syphilis
c. Tertiary syphilis
|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.|
|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|
|Signs and symptoms||
Ø informing sexual contacts of diagnosis Ø not sharing needle with other individuals Ø continuing medical supervision
|Description:||A sexually transmitted disease that is highly contagious caused by chlamydial organism|
|Mode of transmission:||2 -3 weeks for males|
|Incubation period:||Sexual intercourse|
|Signs and symptoms||
|Diagnostic procedure||Culture of aspirated material from vaginal, anal or penile discharges|
|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.|
|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||
|Diagnostic procedure||culture of obtained specimen|
BIOTERRORISM AND PANDEMICS Ø 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.
|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||
|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.|
|Mode of transmission:||
|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|
|Mode of transmission:||Airborne|
|Incubation period:||7 – 10 days|
|Signs and symptoms||