Communicable Disease Nursing

Mr. Regie P. De Jesus, MAN

Communicable Disease

is an illness due to an infectious agent or its toxic products which is easily transmitted or communicated directly or indirectly from one person or animal to another

Communicable Diseases
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

Communicable Diseases

About 60% of deaths caused by communicable diseases can be attributed to: HIV/AIDS Malaria Tuberculosis Measles Diarrheal disease Acute respiratory infection

INFECTIOUS DISEASE

Dengue Fever, H-Fever, Dandy Fever, Breakbone Fever, Phil Hemorrhagic fever
Acute Febrile Disease Flavivirus, dengue virus 1,2,3,4, Chinkungunya Virus, Onyungyong Virus Incidence: Rainy season, urban areas IP: 3 to 10 days ( average 4-6 days) ** Life span of the mosquito is 4 months

Dengue Fever, H-Fever, Dandy Fever, Breakbone Fever, Phil Hemorrhagic fever
THE DISEASE PRESENTS WITH FEVER AND HEMORRHAGIC MANIFESTATIONS AND LABORATORY FINDINGS OF THROMBOCYTOPENIA AND HEMOCONCENTRATION Pathogenesis 1. increased capillary fragility d/t immune complex reactions 2. thrombocytopenia d/t faulty maturation of megakaryocytes 3. decreased blood clotting factors

Vector- Aedes aegypti

- Day

biting mosquito ( they appear 2 hours after sunrise and 2 hours before sunset. Low flying ( Tiger mosquito white stripes, gray wings ) - Breeds on clear stagnant water

CRITERIA FOR DIAGNOSIS:

Fever

,acute, high continuous, lasting for 2-7 days

Positive

torniquet test Spontaneous bleeding (petechiae,purpura,ecchymoses,epistaxis ,gum bleeding, hematemesis, melena) Laboratory: thrombocytopenia </= 100,000mm3, hemoconcentration- an increase of at least 20% in the hematocrit or its steady rise

Assessment: Tourniquet test (Rumpel Leades test) screening test, done by occluding the arm veins for about 5 minutes to detect capillary fragility.
Keep cuff inflated for 6 10 minutes ( child); 1015 minutes ( adults) Count the petechiae formation 1 square inch ( 20 petechiae/sq.in)(+)TT

Platelet count ( decreased) confirmatory test

Classification of Dengue Fever according to severity

Grade I Dengue fever, saddleback fever plus constitutional signs and symptoms plus positive torniquet test Grade II Stage I plus spontaneous bleeding, epistaxis, GI, cutaneous bleeding Grade III Dengue Shock Syndrome, all of the following signs and symptoms plus evidence of circulatory failure Grade IV Grade III plus profound shock and massive bleeding, undetectable BP and pulse

Laboratory criteria DHF: Platelet count Thrombocytopenia <100,000 Hct increased by 20 % or more

1st 2 clinical criteria plus 2 laboratory criteria or rising Hct DHF( dengue hemorrhagic fever) Shock w/ high hematocrit and marked thrombocytopenia DSS ( dengue shock syndrome)

Other : PT (Prothrombin Time) Normal range is 11-16 seconds APTT (Activated Partial Thromboplastin Time) Normal range is 30-45 seconds. Bleeding time Coagulation time Period of communicability pts. are usually infective to mosquito from a day before the febrile period to the end of it The mosquito becomes infective from day 8 to 12 after the blood meal & remains infective all throughout life

pathophysiology
DHF
Febrile phase 2-7 days
First 2 days Vascular injury Plasma leakage (+) petechiae , (+) TT

Dengue Fever Vector caries virus (AEDES aegypti) Bite host ( IP 3-10d)
s/sx : Fever , headache, myalgia ,anorexia Vomiting, sorethroat, rashes

IMPROVE

3rd day WBC, PLT Ct , Hct >20% (+) Pleural effussion

Dengue progress

Circulatory failure
-hypotension -narrow pulse pressure ,20mm Hg (shock)

death

S/sx: Mild dengue abrupt onset of fever, headache, muscle and joint pains, anorexia, abdominal pain. Petecchiae, Hermans rash (5th-7th day; purplish macules w/ blanched areas on extremities) Severe dengue DHF/DSS *TRIAD: fever, rashes and muscle pain Bleeding leading to hypovolemic shock

There is no effective antiviral therapy for dengue fever. Treatment is entirely SYMPTOMATIC Paracetamol for headache ( never give ASPIRIN) IVF for hydration & replacement of plasma BT for severe bleeding O2 therapy is indicated to all patients in shock Sedatives for anxiety & apprehension No IM injections Nasal packing with epinephrine

Medical MX

Nursing Mx

Symptomatic tx Mosquito free environment to avoid further transmission of infection Keep patient at rest during bleeding episodes VS must be promptly monitored For nose bleeding, maintain pts position in elevated trunk, apply ice bag to bridge of nose Observe for signs of shock Restore blood volume ( supine with legs elevated) Gum bleeding soft bristled toothbrush, give ice chips

Dengue hemorrhagic Fever

PREVENTION : DOH 1995 Program

C- hemically treated Mosquito Net L arvae eating fish Gold fish E nvironmental Sanitation 4 0 clock habit A antimosquito soap lanzones peeling N atural mosquito repellant Neem tree , eucalyptus
, oregano

PREVENTION

Cover water drums and water pails at all times to prevent mosquitoes from breeding. Replace water in flower vases once a week. Clean all water containers once a week. Scrub the sides well to remove eggs of mosquitoes sticking to the sides. Clean gutters of leaves and debris so that rain water will not collect as breeding places of mosquitoes. Old tires used as roof support should be punctured or cut to avoid accumulation of water. Collect and dispose all unusable tin cans, jars, bottles and other items that can collect and hold water

Prevention & Control

The 4-S Against DENGUE 1. Search and destroy breeding places of dengue causing mosquitoes such as old tires, coconut husks, roof gutters, discarded bottles, flower vases & other containers that can hold clean stagnant water

2. Self protection measures such as wearing of long sleeve shirts and long pants and using mosquito repellants are a must during daytime.
3. Seek early consultation when early signs such as fever and rashes set in 4. Say NO to indiscriminate fogging except for dengue outbreak

Weils disease, Mud fever, Trench fever, Flood fever, Spirochetal jaundice, Japanese 7 Days fever, Leptospiral jaundice, Hemorrhagic jaundice, Swine Herds disease, Canicola fever a zoonotic systemic infection caused by Leptospira, that penetrate intact and abraded skin through exposure to water, wet soil contaminated with urine of infected animals. Species: L. Manilae, L. Canicola, L. Pyrogens Incubation Period: 6-15 days

Leptospirosis (Weils disease)

Spirochete, Leptospira interrogans, gram (-) Weils syndrome severe form MOT: Contact of skin or open wound from soil water contaminated with urine or feces of infected rats (main host) INGESTION OF CONTAMINATED FOOD/H2O

S/SX: Anicteric Type (without jaundice) manifested by fever, conjunctival infection signs of meningeal irritation + leptospires in the urine Icteric Type (Weil Syndrome) Hepatic and renal manifestation Jaundice, hepatomegally Oliguria, anuria which progress to renal failure Shock, coma, CHF Convalescent Period

Diagnosis

Clinical history and manifestation Culture

Blood: during the 1st week CSF: from the 5th to the 12th day Urine: after the 1st week until convalescent period

LAAT (Leptospira Agglutination Test) other laboratory BUN,CREA, liver enzymes

Treatment

Specific
Penicillin 50000 units/kg/day Tetracycline 20-40mg/kg/day

Non-specific Supportive and symptomatic Administration of fluids & electrolytes Peritoneal dialysis for renal failure

LEPTOSPIROSIS
JAUNDICE IS A BAD PROGNOSTIC SIGN CASE FATALITY RATE : 40%

Blood /vector-borne

Avoidance of exposure to urine & tissues from infected animals ( flood) Rodent Control Hygienic control in slaughterhouses, farmyard buildings & bathing pools Use of protective clothing & boots Immediately wash extremities after possible exposures & disinfect with 705 alcohol Primarily a disease of domesticated & wild animals transmitted via direct or indirect contact. It enters the skin, mucus membrane, conjunctiva Disease is usually short lived & mild but severe infection can damage kidneys & liver Should not donate blood for at least 12 months after recovery

Prevention Control & Nursing Considerations:

Salmonella typhosa or typhi, gram (-) Carried only by humans Bacterial infection transmitted by contaminated water, milk, shellfish ( oyster ) & other foods Infection of the GIT affecting the lymphoid tissue ( Peyers patches) of the small intestine Most severe form of salmonellosis caused by salmonella typhi MOT: oral fecal route 5 Fs : Fingers, Fomites, Flies, Feces, Food & Fluids

Typhoid Fever

Pathophysiology
Oral ingestion Penetrates the intestinal lymphatics, mesenteric Reticuloendothelial system (lymph node, spleen, liver) Bloodstream

Peyers patches of SI

necrosis and ulceration

Typhoid Fever Ulceration of the Peyer's Patches

Typhoid Fever
Clinical Manifestations: Incubation Period: 1-3 weeks 1. Prodromal 1st week: Step ladder fever 40-41 deg, headache, abdominal pain, GI manifestations 3 cardinal signs of pyrexial stage: 1.ROSE SPOTS ( rose-colored macules that disappears after applying pressure, found on the chest, abdomen, back, a.k.a. Evanescence rash 2. Remittent fever ( ladder like) 3. Spleenomegaly

Typhoid Fever Rose Spots

2. Fastidial = 2nd week ( Typhoid) a. High fever, typhoid psychosis w/ hallucination, confusion, delirium

Drug of choice: Antibiotics

1. Chloramphenicol 2. Ampicillin 3. Cotrimoxazole

b. Severe abdominal pain c Sordes typhoid state

1st week step ladder fever (BLOOD) 2nd week rose spot and fastidial typhoid psychosis (URINE & STOOL) 3rd week (complications) intestinal bleeding, perforation, peritonitis, encephalitis, 4th week (lysis) decreasing S/SX 5th week (convalescence)

Dx: Blood culture (typhi dot) 1st week Stool and urine culture 2nd week Widal test agglutination test best done during the 8th day (2nd stage)
3 Antigens Being Used (+) Ag O Active typhoid stage (+) Ag H past infection or vaccinated individual (+) Ag Vi common in carriers

Mgmt: Chloramphenicol (DOC) 100mg/kg/day, Amoxicillin, Sulfonamides, Ciprofloxacin, Ceftriaxone ** Observe standard precaution until 3 negative stool culture**

Nursing Interventions
Environmental Sanitation Food handlers sanitation permit Supportive therapy Assessment of complications (occuring on the 2nd to 3rd week of infection ) - typhoid psychosis, typhoid meningitis - typhoid ileitis

Chicken Pox, Varicella

Acute & highly contagious disease of viral etiology Childhood disease & adolescents (adults more severe) Not common in infancy Locally called Bulutong Human beings are the only source of infection CA = Varicella Zoster virus, Herpes virus IP 10-21 days MOT: airborne spread > nose & throat secretions > Vesicles ( contagious in early stage of eruption

Prodromal period: headache , vomiting, fever Papulovesicular rashes appear on trunk spreading to face and extremities (CENTRIFUGAL)
Macules

papules vesicles with clear fluid inside crusting and scar formation

The

disease is communicable until the last crust disappear ( D1 before D6 after appearance of rashes)

Period of Communicability 5 days before rashes & 5 days after rashes crusting - dry

Rashes: Maculopapulovesicular (covered areas), Centrifugal rash distribution, starts on trunk and spreads to entire body

Leaves a pitted scar (pockmark)

CX = secondary bacterial infection, furunculosis, pneumonia, meningoencephalitis ( rare)

Dormant: remain at the dorsal root ganglion and may recur as shingles (VZV)

Curative & Nursing Considerations:

If it feels itchy, give oral antihistamine or local antihistamine Avoid rupture of lesions Cut nails short/ mittens Pay attention to nasopharyngeal secretions/ discharges Disinfection of linen ( sunlight or boiling) Prophylactic antibiotics

Treatment:
a. oral acyclovir (Zovirax) slow down multiplication b. Tepid water and wet compresses for pruritus oatmeal bath for pruritus, baking soda + warm water to promote drying c. Potassium Permanganate (ABO) a. Astringent effect b. Bactericidal effect c. Oxidizing effect (deodorize the rash)

Exclusion from school for 1 week after eruption appears An attack gives lifetime immunity. Second attack is rare Immunoglobulins can be given ( 12 mos) Drug of choice: Acyclovir ( Zovirax ) topical cream applied to crusts

Preventive measures

Active immunization with LIVE

ATTENUATED VARICELLA VACCINE

Start at 1 yr old ( 1 dose ) booster 4-12y If >13 yrs = 2 doses Given SC

Avoid exposure as much as possible to infected person

Pulmonary Tuberculosis( Kochs Disease/Pthisis/Consumption disease)

CA: Mycobacterium tuberculosis ( bacteria), acid fast bacilli The organism multiplies slowly & is characterized as acid fast aerobic organism which can be killed by heat, sunshine, drying & ultraviolet light. Sputum of persons with TB is the most common source of the organism spread through droplet ( airborne) Potts disease thoracolumbar Milliary TB kidney, liver, lungs

Is a chronic, or subacute or acute respiratory disease commonly affecting the lungs characterized by formation of tubercles in the tissues which tend to undergo caseation, necrosis and calcification. IP: 2 10 weeks Mode of Transmission: Direct: droplet ( sneezing, coughing) Indirect: continuous exposure to infected persons within the family Source of Infection:sputum, blood from hemoptysis, nasal discharges and saliva
-

Classification :
Minimal slight lesion, small part of lobe/ lungs Moderately advanced one or both lung may be involved Far advanced- more extensive

Clinical classification:

1. inactive TB
Symptoms absent Sputum negative CXR no evidence of cavity

2. Active
Tuberculin test positive CXR progressive (+) of symptoms Sputum (+)

3. Activity not determined

Clinical manifestation:
Afternoon rise of temperature for 1 mo. or more Body malaise, weight loss Cough, dry to productive (>2-3 weeks) Dyspnea, horseness of voice Hemoptysis pathognomonic Occasional chest pain Night sweating (+) sputum for AFB

PD 996 Compulsory Immunization below 8 years ( 0 -7 yrs) Proclamation # 6 WHO Universal Child Immunization

Etiologic Factors that contribute heavily to the high Incidence & high mortality rate of TB: Poverty / Overcrowded homes Protein undernutrition Deficiencies in Vit A,D,C Children below 5 years old prone to infection due to inadequate levels of immunity

DX

1. Case Finding:
A. Sputum Microscopy ( cheapest ) Results take about 3 weeks to confirm Sputum sample shld be taken 1st thing in the morning upon arising 3 specimens: 1st on the spot = HC 2nd- upon arising = Home 3rd on the spot = HC

2. Sputum Culture & Sensitivity Confirmatory 3. Chest X-ray extent of damage 4. Tuberculin Test
1. PPD Purified Protein Derivative Mantoux Test- (more reliable) = ID injection of tuberculin extract into the inner aspect of forearm to detect infection/exposure to CA. Localized reaction- detected in 48 to 72 hours (+) induration of 10 mm or above Immunocompromised = >5mm ONLY Exposure

Tuberculin test. Erythema and induration at site of intradermal injection of 5 tuberculin units in a child with primary tuberculosis. This is an unusually severe reaction. Mantoux method.

CATEGORIES OF TB

category I (new PTB) - (+) sputum(+) chest xray category II (PTB relapse not less than 6 mos)

category III (active PTB case) - (-) sputum (+)chest xray, regression of infiltrates Category 1V partially treated; poor compliance to DOTS Category V PTB suspect ( (+) skin test; (+) family member with PTB

Management: short course 6-9 months long course 9-12 months DOTS- directly observe treatment short course

* 2 wks after medications non communicable 3 successive (-) sputum - non communicable rifampicin or INH- prophylactic

Primary Anti TB Drugs

1. Rifampicin = SE = orange colored urine, GI upset, Jaundice, Renal failure, thrombocytopenia

Primary Anti TB Drugs

2. Isoniazid (INH) = ( Bacteriostatic) inhibits ( Bactericidal ) kills Used prophylactically to patients (+) of PPD SE = Rashes (give anti-histamine); Peripheral neuritis ( Give Vit B6- Pyridoxine)50 mg; Jaundice Hepatotoxicity

3. Pyrazinamide ( PZA) SE = Hyperuricemia ( inc uric acid) Mx: Inc fluid intake 4. Ethambutol = 15-20mg/day SE = Optic neuritis ( dec visual acuity) Give Vit. B6(Pyrdoxine) 5. Streptomycin SE = Ototoxicity, 8th cranial nerve damage

( Tinnitus, dizziness, N&V)

MDT side effects r-orange urine i-neuritis and hepatitis p-hyperuricemia e-impairment of vision s-8th cranial nerve damage

TREATMENT:

CATEGORY 1 - NEW PTB, (+) SPUTUM GIVE RIPE 2 MONTHS, MAINTENANCE OF RI 4 MONTHS

CATEGORY 2 - PREVIOUSLY TREATED WITH RELAPSES GIVE RIPES 1ST 2 MONTHS, RIPE 1 MONTH, MAINTENANCE RIE 5 MONTHS
CATEGORY 3 - NEW PTB (-) SPUTUM FOR 3X GIVE RIPE 2 MONTHS, MAINTENACE RI 2 MONTHS CATEGORY 4 - REFER

* IF RESISTANT TO DRUGS GIVE ADDITIONAL MONTH/S AS PRESCRIBED

PTB- NURSING MANAGEMENT

1.

2.
3. 4.

5. 6. 7. 8. 9. 10.

MAINTAIN REPIRATORY ISOLATION Administer medicine as ordered Always check sputum for blood or purulent expectoration Encourage questions and conversation so that the patient can air his or her feelings Teach or educate the patient all about PTB Encourage patient to stop smoking Teach how to dispose secretion properly Advised to have plenty of rest and eat balanced diet Be alert of drug reaction Emphasize the importance of follow-up

PULMONARY TUBERCULOSIS ( Kochs Disease/Phthisis/ consumption Disease)

PREVENTION: 1. Submit all babies for BCG immunization 2. Avoid overcrowding 3. Improve nutritional and health status 4. Advise persons who have been exposed to infected persons to receive tuberculin test if necessary CXR and prophylactic isoniazid.

Pyromidium Bahamense ( Algae), Dinoflagellates Plankton Ingestion of Saxitoxin in contaminated bi-valve shellfish Saxitoxin binds w/ Na channels leading to loss of skeletal muscle excitability IP 15 min- 12 hrs S/sx: Circumoral and extremity numbness, nausea and vomiting, headache ( bec of the toxins),dizziness, muscle and respiratory paralysis, rapid pulse, difficulty of speech Dx: history Mgmt: emesis/gastric lavage + activated charcoal, supportive

Paralytic shellfish Poisoning Red Tide Poisoning

Paralytic shellfish Poisoning Red Tide Poisoning

Dx: history Mgmt: 1. Induce vomiting (gastric lavage + activated charcoal) 2. Drink pure coconut milk ( weakens toxins) in the early stage 3. Give NaHCO3(25 mgs) in glass of water 4. Avoid using vinegar in cooking shellfish affected by red tide ( 15x increase when mixed with acid) 5. Toxin of red tide is not totally destroyed in cooking 6. Avoid eating tahong , halaan, Kabiya, abaniko during red tide season 7. No specific medicines