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Communicable Disease Final
Communicable Disease Final
canicola Period of communicability: none but leptospira are found in the patients urine between 10 to 20 days after onset INCUBATION PERIOD: 6 to 15 days
Definition:
DISEASE,CANICOLAFEVER) - infection carried by animal both domesticated and wild whose excreta is contaminated or food which is ingested or inoculated thru skin or mucus membrane
(WEILS DISEASE, MUDFEVER, SWINEHERDS
Clinical Manifestation s
muscle aches, eye pain with bright lights, followed by chills and fever. Watering and redness of the eyes occurs
PATHOPHYSIOLOGY
Predisposing Factor: Dirty environment, age, seasons, males, geographic areas Rodents, wild animals Infected urine or carcasses Man Incubates for 6 to 15 days Profileration and widespread dissemination Organ systems are affected Leptospirosis Complications: Pneumonia Optic Neuritis Peripheral neuritis
DIAGNOSTIC EXAM
total WBC count slightly elevated with neutrophilia. Rising titer of leptospiral antibodies is found from the second week onwards. Increased erythrocyte sedimentation rate i (about 60 mm). throbocytopenia
MEDICATIONS
PENICILIN G drug of choice.
TETRACYCLINES (Doxycycline)
Nursing Management:
isolation of patient: urine must be properly disposed Darken the patients room because light is irritating to the eyes of the patient. Observe meticulous skin care to ease pruritus. health teachings: keep a clean environment
Disease Process CAUSATIVE AGENT: Neisseria meningitidis ( other strains: Haemophilus influenza common in young children, Streptococcus pneumonia common in adults, Straphylococcus aureus ) PERIOD COMMUNICABILI TY -until meningococci are no longer present in the mouth and nasal discharges. INCUBATION PERIOD : 3 6 days MODE OF TRANSMISSION : respiratory droplets
Definition:
PATHOPHYSIOLOGY
bacteria
Increased body temperature and increased WBC count crossing to the blood-brain barrier (since it has no WBC for immunity infection progresses) meninges, inflammatory response /reaction Edema in the meninges affects the intracranial nerves Brudzinzkis sign Kernigs sign ,Photophobia
Clinical Manifestation s NUCHAL RIGIDITY pathog nomon ic sign Neck shoulder and back stiffness Opisthotonus Positive Kernig and Brudzinskis sign
Clinical Manifestation s MEDICATIONS Mild fever and malaise Mannitol Rash start from the truck Dexamethason and spread to e other parts, progression Dilantin/pheny completed in 6 totoin 8 hours macule Pyretinol/ence lesion that is flat phabo L papule an elevated lesion vesicle filled with clear fluid crust a scab lesions caused by secretions of a vesicle drying on the skin pustule vesicle affected and filled with pus
DIAGNOSTIC EXAM: Disease Process CBC with differentialelevated white blood cell count, neutrophils Blood cultures- may MODE OF indicate organism TRANSMISSIO Lumbar puncture with CSF cultures- elvated N: direct thru cell count, may indicate droplet organism
Nursing Management:
Isolate the patient quiet and darkened room Prevent stress provoking factors Prevent injury during episodes of convulsions Maintain fluid and electrolyte balance Provide balanced diet, low fat
infection or airborn; indirect thru linen and fomites. INCUBATION PERIOD : 10 to 21 days
Definition: -Highly contagious disease caused by herpes virus characterized by vascular eruptions on the skin and mucous membrane.
PATHOPHYSIOLOGY
Inhalation of contaminated respiratory droplet Infection in the conjunctivae or the mucosa of the upper respiratory tract Viral proliferation in regional lymph nodes Primary viremia 2nd viral replication in the internal organs Secondary viremia Infection of cells of the malpighian layer Intercellular & intracellular edema/vesicles Pre-eruptive manifestations; Mild fever and malaise. Eruptive stage; Rash starts from the trunk., Appearance of rashes through following stages: macule, papule, vesicle, pustule, crust, All stages are present simultaneously before all are covered with scabs, known as Celestial map.
DIAGNOSTIC EXAM:
Examination of vesicle fluid under Disease Process electron 2 TYPES OF microscope( shows RABIES VIRUS: round particles a. STREET VIRUS) - natural virus the Scrapings of invading /the vesicles floor of transmitted in the colored by Giemsa. saliva ( Tzanck smear ) b. FIXED VIRUS shows do(not usually multinucleated invade the salivary giant cells glands with ) constant Four fold rise in incubation period antibody titre of Detection of viral 4 to 6 days DNA by PCR INCUBATION Fluorescent PERIOD: Antibody to a.In dogs and cats 1 week to 7 Antigen Membrane month b.In man - 4 to 8 weeks MODE OF TRANSMISSION: contamination of a bite/scratch or other break in the skin from saliva
Nursing Management:
Isolation until crust have fallen off Calamine lotion over rashes Antipyretics for fever. Handwashing and cutting of fingernails
MEDICATIONS Acyclovir/zovirax Diphenhydramine (Benadryl) Clinical Manifestation s >Presence of NEGRI BODIES in brain tissues (round or oval bodies found in the cytoplasm of neurons in animal with rabies
Definition:
(LYSSA, HYDROPHOBIA ) - severe viral infection of the CNS that is communicated to human in the saliva of infected animals or human caused by rabies virus (RHABDOVIRUS) filterable virus and inactivated by sunlight
PATHOPHYSIOLOGY
Rabies virus transmission via animal bites Virus travels along the nerves to the spinal cord and to the brain Virus multiplication happened Travels alomg other nerves to the salivary glands and into the saliva Short period of depression, restlessness, malaise and fever Paralysis in the lower legs, spasm of the muscles, in the throat and voice box Disease Process MODE OF TRANSMISSION: Coma and death
MEDICATIONS
LYSSAVA VERORAB
thru bites of an 1. infected of exposure History mosquito bites 2.Parenterally 2. Development of blood transfusion characteristic or contaminated symptoms syringes and 3. Microscopic exams needles presence of NEGRI BODIES in brain tissue 3.Mingling of and saliva maternal infected 4. Flourescentthat of blood with rabies antibody (fra) techique the infant during delivery 4.Transplacental ( congenital malaria ) very rare INCUBATION PERIOD (varies depending on greater or lesser resistance of individual )
Nursing Management:
Treatment of wound with soap and water or zephiran betadine Isolate patient provide restful, quiet and semi dark environment Cover IVF with paper bag no sight of water Provide comfort
Definition:
( MARSH FEVER) - an acute or chromic disease caused by protozoa plasmodia transmitted to man by the bite of infected female anopheles mosquito ( Anopheles minimus flavirostris ) which is a night biting and breeds in flowing clear and shaded stream
Clinical Manifestation s A.PRODROMA L PHASE P. falciparum fatigue, vague abdominal pains, muscle aches, highly colored urine, orthostatic hypotension, hepatomegaly an spleenomegaly P. vivax headache, photophobia, muscle aches, anorexia, nausea and vomiting P. ovale and P. malariae not significant
PATHOPHYSIOLOGY
female Anopheles mosquito bites, injecting saliva containing sporozoites sporozoites enter liver cells and multiply sporozoites change to merozoites merozoites are released from the liver and enter the bloodstream merozoites attack red blood cells multiply in RBCS RBCs burst and release the merozoites which invade other RBCs and cause recurring chills and fever
MEDICATIONS
4 Aminoquinolines (Choloroquine, Aminodiaquine and Quimine ) Primaquine pyrimethamineSULFADOXINE (FANSIDAR) safest during pregnancy.
Disease Process urine reveals small common in amounts of protein children 6 months to 5 years ( rare liver function tests below 6 mos. due reveals elevated to immunity transaminase level and passed from the increasemother ) in indirect serum bilirubin MODE OF TRANSMISSION: 1.Direct contact of mouth secretions 2.Indirect thru toys an clothing that are contaminated INCUBATION PERIOD: 2 to 6 days PERIOD OF COMMUNICABILI TY 1 to 2 days in treated patients
DIAGNOSTIC EXAM:
NURSING MANAGEMENT: Isolation Supportive care PREVENTION: Eliminate breeding places of mosquitoes Advise travelers of high risk areas Screening of windows
Clinical Manifestation s Pathognomonic sign: Pseudomembra ne Irritating nasal discharge usually serosanguenous Bullneck apperance Dyspnea
Definition:
characterized by formation of pseudomembranre commonly in the faucial area and tonsils by the exotoxin produced by Corynebacterium diphtheriae (KLEBSLOEFFLER BACILLUS)
PATHOPHYSIOLOGY
causative agent : Cornybacteruim diptheriae Enters the body via direct and indirect contact Produces exotoxin Absorbed into the mucous membranes Causes destruction of the epithelium Inflammatory response takes place Accumulation of inflammatory cells, necrotic epithelial cells, and organism debris, which form the characteristic adherent grey pseudomembrane Attempts to remove the pseudomembrane result in bleeding and expose an inflamed
MEDICATIONS
NURSING MANAGEMENT:
CBR prevent complications Oral hygiene Maintain fluids an d electrolytes Adequate nutrition Ice colar relieve pain
s diameter-
Disease Process
PATHOPHYSIOLOGY B. pertussis is transmitted by droplets Attach to pharyngeal epithelial cells Release number of antigens, toxins, and other substances Triggers the immune system nasopharyngeal secretions,wheezing and cough DIAGNOSTIC EXAM
Nasal swab and sputum cultures shows B. pertussis only WBC-is usually increased fluorescent antibody screening of nasopharyngeal smears- positive for Pertussis
NURSING MANAGEMENT
CBR Increase fluid intake not during attacks Abdominal binders to prevent abdominal hernia No large nipples to prevent aspiration No feeding during attacks Strict isolation High calorie/ bland diet Proper positioning PATHOPHYSIOLOGY
Repeated close contact w/ infected,Occupation,Indefinite substance abuse via IV,recurrence of infection Exposure or inhalation of infected Aerosol through droplet nuclei (exposure to infected clients by coughing,sneezing, Definition: talking) Tubercle bacilli invasion in the apices of the is a bacterial near the pleurae of the lower lobescalled Lungs or infection caused by a germ Mycobacterium tuberculosis. The bacteria usually Bronchopneumonia develops in the lung tissue attack the lungs, but they can also damage other Necrotic Degeneration occurs parts of the body drainage of necrotic materials into the tracheobronchial tree Lesions may calcify (Ghons Complex) and form scars and may heal over a period of time Tubercle bacilli immunity develops Acquired immunity leads to further growth of bacilli and development of active infection Dyspnea, chest tightness, hemoptysis, crackles Non-productive/productive cough. Hemoptysis Chest pain Chest tightness
Clinical Manifestation s
general malaise, anorexia , easy fatigability, apathy, irritability, indigestion tachycardia, dyspnea, cyanosis fever late in the afternoon night sweats acute exudates involvement ( advanced cases ) loses weight malaise hemoptysis
Disease Process Tuberculosis: CAUSATIVE AGENT: Mycobacterium tuberculosis MODE OF TRANSMISSION: droplet infection INCUBATION PEROID: 2-10 weeks
DIAGNOSTIC EXAM:
Sputum acid fast bacilli staining RESULTS OF SPUTUM MICROSCOPY O negative for bacilli +- 1 4 bacilli ++- 5 10 bacilli +++ - 10 20 bacilli ++++ more than 20 bacilli Chest x-ray mantoux test
NURSING MANAGEMENT
CBR adequate nutrition ambulatory chemotherapy npo hemoptysis oxygen inhalation blood transfusion coagulants - vit. k and hemostan PATHOPHYSIOLOGY Predisposing factor: Bite of aedes aegypti mosquito carrying a virus Definition: Virus goes into the circulation acute tropical cells and characterized by severe pain in Infect disease general cellular response the eye and in the joints and bones an accompanied
Disease Process MODE OF TRANSMISSION: bite of an infected Aedes aegypti mosquito which is day biting with limited flying movement INCUBATION PERIOD: 4 to 6 days HEMORRHAGIC FEVER is a result of: Increase capillary fragility strong immune complex reaction that produce toxic substance like histamine, bradykinin, which damage capillary wall
by an initial erythema caused by dengue virus and Initiates destruction on the platelet transmitted by mosquito Aedes aegypti
Potential for haemorrhage Stimulates intense inflammatory response Release of exogenous pyrogens Increase WBC (Neutrophils and macrophages) Release of endogenous pyrogens Reset of hypothalamic thermostat fever
Clinical Manifestation s
Sudden onset of hyperpyrexia and headache, patient is flushed and acutely ill Anorexia, nausea and vomiting severe abdominal pain and tenderness Hepatomegaly 50 to 60 % of cases
DIAGNOSTIC EXAM:
Positive tourniquet test ( rumpel leed test ) increase capillary fragility. hematologic exam decrease Platelet determination count (150,000 to 400,000/cu.mm ) Hemagglutinationinhibition test most frequently used Disease Process
NURSING MANAGEMENT
Epistaxis ice compress on bridge of nose, let patient bite something Gum bleeding ice chips, bristle toothbrush GI bleeding observe signs of bleeding, place o NPO. Avoid highly seasoned food DO NOT GIVE ASPIRIN causes platelet degeneration and may cause further bleeding.
Definition:
infectious disease caused by an anaerobic bacteria(cannot leave in the presence of oxygen) which produces a potent exotoxin
Clinical Manifestation s >lockjaw or trismus >boardlike abdomen >photophobia eyes partially close >laryngeal / pharygeal spasm >irritability and restlessness >convulsions
MODE OF TRANSMISSION direct and indirect contamination of wound, umbilical stump in newborn INCUBATION PEROD: 3 days to 3 weeks with average of 10 days PERIOD OF COMMUNICABILI TY: not transmitted persons to person directly
2 FORMS:
PATHOPHYSIOLOGY deep penetrating wound Clostridium tetani Produces the neurotoxin tetanospasmin(TS) at the site of tissue injury TS binds to the motor nerve ending and then moves by retrograde axonal transport to the CNS binds to GABA and blocks presynaptic release of GABA muscle spasm
MEDICATIONS
DIAGNOSTIC EXAM:
CSF is normal Blood exam normal or Disease elevated slightly Process WBC ct.
Incubation Period: The incubation period is 50 to 189 days or two to five months with a mean equal to 90 days. Period of Communicability: latter part of the incubation period and during the acute phase. The virus may persist in the blood for many years. Mode of Transmission: Hepatitis B can be directly transmitted by person to person contact via infected body fluids. It can be transmitted though contaminated needles and syringes. Transmission can occur through infected blood or body fluids introduced at
NURSING MANAGEMENT
Proved quiet semi dark environment
Minimal handling Prepare tongue depressions Maintain an adequate airway Closely guard the patient Support during spasm and convulsions No restraints Adequate fluid and electrolytes High calorie liquid to soft diet
Clinical Manifestation s Fever, malaise, and anorexia. Nausea, vomiting, abdominal discomfort, fever and chills. Jaundice, dark urine, and pale stools.
PATHOPHYSIOLOGY
the virus enters a new host infect liver cells (hepatocytes) inflammation decrease liver function scarring or fibrosis occurs Fever, malaise & anorexia, Nausea, vomiting, abdominal discomfort, fever and chills, Jaundice, dark urine, and pale stools. Fulminant hepatitis; Fatal and manifested by severe symptoms such like ascites and bleeding
MEDICATIONS
DIAGNOSTIC EXAM:
elevated serum transferase levels, AST and ALT low blood levels of albumin an abnormally long prothrombin time
NURSING MANAGEMENT
Encourage frequent small feedings of highcalorie, low-fat diet encourage eating meals on a sitting position to decrease pressure on the liver monitor intake and output provide frequent oral fluids as tolerated promote periods of rest during symptomatic phase
Disease Process
Definition:
Clinical Manifestation s
change in skin color-either reddish or white loss of sensation on the skin lesion ulcers that do not heal loss of eyebrowmadarosis contractures
PATHOPHYSIOLOGY
EXAM:
PERIOD OF Mean- from COMMUNICABILI mucocutaneous lesions TY : as long as there are open Lepromin Skin Test lesions has cross sensitivity to tuberculosis infection and BCG vaccination Mitsuda Reaction more useful for the determination of the type of disease and prognosis
M. Leprae attacks the peripheral nerves Ulnar, radial, posterior-popliteal, anteriortibial, and facial nerves Bacilli damage the skins fine nerves Cause anesthesia, anhidrosis, and dryness If they attack a large nerve trunk, motor nerve damage, weakness, and pain occur Peripheral anesthesia, muscle paralysis, atrophy
MEDICATIONS
Dapsone (Avlosuflon) Rifampin (Rifadin) Clofazimine (Lamprene) Minocycline (Minocin)
NURSING MANAGEMENT
Isolation Maintain balance nutrition, sleep and rest Help the family to understand and accept to remove social stigma Good personal hygience Handling of infants and young ones should be avoided
Definition:
Disease Process
MODE OF TRANSMISSION : airborne droplet nuclei or close contact INCUBATION PERIOD: 10 to 21 days PERION OF COMMUNICABILI TY: entire course of illness
Clinical Manifestation s fever and malaise lymphadenopat hy Eranthem: discrete rose spots on soft palate Exanhem: Variable; begins on face spreads quickly over entire body
PATHOPHYSIOLOGY Contact with the infected person Maternal viremia Fetal viremia Disseminated infection involving many fetal organ Intrauterine growth retardation, blueberry muffin skin, lethargy and hypothermia Causative agent spreads through the cells and the
DIAGNOSTIC EXAM:
Hemagglutinationinhibition test (hi) Complement fixation test (cf) ELISA ( Enzyme Linked Immunosorbent Assay )
blood
Mild feverish illness associated with rash and aches and joint
MEDICATIONS
NURSING MANAGEMENT
darkened room to relieve photophobia diet: should be liquid but nourishing warm saline solution for eyes to relieve eye irritation for fever: TSB and antipyretics prevent spread of infection, respiratory inhalation
Disease Process Direct transmission, when an infected person sneezes mucus directly into the eyes, nose or mouth of another person Airborne route, when someone inhales the aerosols produced by an infected person coughing, sneezing or spitting Hand-to-eye, hand-to-nose, or hand-to-mouth transmission, either from contaminated surfaces or from direct personal contact such as a DIAGNOSTIC hand-shake EXAM:
Definition:
is a viral infection that affects mainly the nose, throat, bronchi and, occasionally, lungs. Infection usually lasts for about a week, and is characterized by sudden onset of high fever, aching muscles, headache and severe malaise, nonproductive cough, sore throat and rhinitis.
Clinical Manifestation s
Fever and extreme coldness (chills shivering, shaking (rigor)) Nasal congestion Body aches, especially joints and throat Fatigue Irritated, watering eyes Reddened eyes, skin nose etc Petechial Rash
PATHOPHYSIOLOGY
virus attaches to host viral RNA enters host cell viral RNA replicates within host cell new virus particles are released and assembled binding and destruction of epithelial cells from nasopharynx and alveoli local inflammatory response systemic body reaction (fever, muscle pain etc.)
MEDICATIONS
Amantadine (symmetrel) rimantadine (flumadine) oseltamivir (Tamiflu) zanamivir (Relenza)
NURSING MANAGEMENT
administer analgesics, antipyretics, and decongestants, as ordered. Follow droplet and standard precautions. Provide cool, humidified air but change the water daily to prevent pseudomonas superinfection. Encourage the patient to rest in bed and drink plenty of fluids. Administer I.V. fluids as ordered. Administer oxygen therapy if warranted. Regularly monitor the patients vital signs, including his temperature.
Definition:
Disease Process ( RUBEOLA ,7 DAY MEASLES, MORBILLI, & RED MEASLES ) -Contagious exanthematous disease of acute onset -Caused by measles virus ( paramyxovirus filterable virus )
MODE OF TRANSMISSION : -droplet infection OR AIRBORNE. -indirect thru contaminated articles with respiratory secretions INCUBATION PERIOD: 10 to 22 days PERIOD OF COMMUNICABILI TY : 5h day of incubation period until the day of the rash DIAGNOSTIC
Clinical Manifestation s anorexia and irritability pruritus lethargy KOPLIK SPOTSpathognomonic sign eruption on the skin; maculopapular rashes (red in color )
PATHOPHYSIOLOGY measles virus transmitted via droplet s infects epithelial cells of the nose and conjuctivae virus multiplies extends to regional lymph nodes continues to replicate on epithelial and reticuloendothelial infections become established on the skin and other tissues including the respiratory tract Kopliks spot may develop in buccal mucosa rashes develop virus can be found in bone, skin, respiratory tract and other organs viraemia gradually decreases viraemia and presence of virus in tissue and NURSING MANAGEMENT organs ceases SYMPTOMATIC AND SUPPORTIVE Eye-care wash face and avoid direct sunlight Oral hygiene Skin-care no strong soaps and alcohol Anti-pyretics for fever Hypoallergenic diet Vitamin A as ordered to protect the epithelial lining of the resp. tract, GIT and eyes.
EXAM:
multinucleated giant cells in smears of nasal mucosa low white blood cell count and relative lymphocytosis in PB measles encephalitisraised protein, lymphocyte in CSF
MEDICATIONS
Catanduanes State Colleges COLLEGE OF HEALTH SCIENCES Department of Nursing Virac, Catanduanes
Submitted by: Patricia Dawn G. Molina BSN 3A Submitted to: Dr. Alvin C. Ogalesco Ed.D Professor