GERMAN MEASLES

(RUBELLA/THREE-
DAY MEASLES
Prepared by:
Jett Randall C. Atienza
 DEFINITION
 German Measles is a mild viral
illness caused by Rubella Virus.
 It causes mild feverish illness
associated with rashes and
aches in joints.
 It has teratogenic effect on the
fetus.
INFECTIOUS AGENT

Rubella Virus
( Family-
Togaviridae; Genus-
Rubivirus )
 INCUBATION PERIOD
 From exposure to the
appearance of rash, the
incubation period is
usually 14 to 21 days.
 PERIOD OF
COMMUNICABILTY
 The virus is communicable
approximately 1 week before and 4
days after the onset of rashes, but is
at it’s worst when the rash is at it’s
peak.
 Highly communicable infants with
congenital rubella may shed virus for
months after birth.
MODE OF TRANSMISSION
 Direct contact with nasopharyngeal
secretions
 Air droplets
 Transplancental transmission in
congenital rubella.
 Infants with congenital rubella shed large
quantities of virus in their pharyngeal
secretions and urine which serve as
source of infections to other contacts.
 CLINICAL MANIFESTATIONS
PRODROMAL PERIOD
Low
 grade fever
Headache


Malaise


Mild coryza


Conjunctivitis


Post auricular, sub- occipital and posterior cervical


lymphadenopathy which occur on the 3rd to 5th day
after onset
CLINICAL MANIFESTATIONS
 ERUPTIVE PERIOD
 A pinkish rash on the soft palate (Forshheimer’s
spot)
 Eruptions appears after the onset of adenopathy
 Children usually present less or no constitutional
symptoms
 Rash may last from one to five days
 Testicular pain in young adults
 Transient polyarthralgia and polyarthritis may occur
in adults and occasionally in children.
MODALITIES OF TREATMENT

 Very little treatment is necessary;

it is essentially symptomatic.
 COMPLICATIONS
 Encephalitis
 Neuritis
 Arthritis
 Arthralgias
 Rubella syndrome, manifested by:
 Microcephally
 Mental retardation
 Cataract
 Deaf-mutism
 Heart disease
 RISK OF CONGENITAL
MALFORMATION
 100 Percent-when maternal infection occurs on
the first trimester of pregnancy or first month
of gestation
 4 percent-in the second and third trimester of
pregnancy
 90 percent of congenital rubella cases will
excrete the virus at birth are therefore
infectious.
 10 percent-the virus remains contagious until
one year of age of an infected child.
 PATHOGENESIS
 Maternal viremia

 Placental infection

 Fetal viremia

 Disseminated infection involving many fetal

organs
 NURSING MANAGEMENT
 The patient should be isolated.
 The patient should be advised to rest in bed until fever
subsides.
 Patients room must be darkened to avoid photophobia.
 The patient must take mild liquid but nourishing diet.
 The patients eyes should be irrigated with warm normal
saline to relieve irritation.
 The ears must be taken care of. Do not apply heat or
cold compress unless it is ordered.
 Good ventilation is necessary.
 The spread of infection must be prevented.
 The occurrence of the complications must also be
prevented.
 PREVENTION
 Administration of live attenuated
vaccine (MMR- Measles, mumps
and Rubella Vaccines)
 Pregnant woman should avoid
exposure to patients infected with
Rubella Virus
 Administration of Immune Serum
Globulin 1 week after exposure to
Rubella
HEPATITIS
HEPATITIS A/ INFECTIOUS
HEPATITIS/ CATARRHAL
JAUNDICE
 DEFINITION
 A liver disease caused by hepatitis A
virus. This is an inflammation of the liver
that is not that severe and runs on acute
course.
 This generally starts within 2 to 6 weeks
after contact with the virus, and lasts no
longer than 2 months.
 It is known as infectious hepatitis
because its spreads relatively easy from
those infected to closed contact.
 INCUBATION PERIOD

 Ranges from 15 to 60 days or 3 to 5

weeks.
 With a mean incubation period of 30
days.
 PERIOD OF
COMMUNICABILITY

 The infected patient is capable of

transferring the organism a week
before and a week after the
appearance of symptoms.
 MODE OF TRANSMISSION
 Ingestion of contaminated drinking
water or ice, uncooked fruits and
vegetables, and fruits and vegetables
grown in washed with contaminated
water.
 Fecal-oral pathway
 Infected food handlers
 WHO CAN TRANSMIT HEPATITIS A
VIRUS?
 Children's diapers and toys
 Homosexual men infection from Oral-
Anal sexual contact.
 Troup’s living under crowded conditions
at military camps or in the field are at
great risk.
 People who lives in areas with sanitary
conditions.
 PATHOGENESIS
 Hepatophilic virus

 Infects the liver

 Interlobular infiltration with mononuclear cells

results in necrosis and hyperplasia of cells

 Failure of the bile to reach the intestine in normal

amount

 Obstructive jaundice
 CLINICAL MANIFESTATIONS
 Flu like illness with chills and high
fever
 Diarrhea, fatigue, and abdominal
pain
 Loss of appetite
 Nausea, diarrhea and fever
 Jaundice and dark colored urine
 COMPLICATIONS
 Encelopathy
 GIT bleeding
 Hyperflexia
 Edema and ascitis
 Aplastic anemia
 In late course of disease, loss of corneal
and pappillary reflexes, elevated
arterial blood, respiratory failure.
 DIAGNOSTIC PROCEDURE
 HAV and HBV- complement fixation rate
 Liver function test- to determine the presence
and extent of liver damage and to check the
progress of the liver
 Bile examination in stool and urine
 SGOT-serum glutamic oxaloacetic
transaminase
 SGPT-serum glutamic pyruvic transaminase
 ALT-serum alanine transminase
 IgM level
 TREATMENT MODALITIES
 There is no specific treatment, although bed rest is
essential.
 Diet must be high in carbohydrates, low in fat, and
low in protein.
 Patient must take vitamins supplement especially
the B complex group.
 Intravenous therapy is occasionally necessary.
 Isoprinosine (methisoprenol) may enhance the cell-
mediated immunity of the T-lymphocytes
 Alkalies, belladonna, and anti-emetics should be
administered to control dyspepsia and malaise.
 NURSING MANAGEMENT
 The patient must be isolated (enteric isolation)
 Patient should be encourage to rest.
 Nutritional status must be improved.
 Appropriate measures to minimize spread of the disease
must be utilized.
 Observed the patient check stool for the presence of blood.
 Provide optimum skin and oral care.
 Increased in ability to carry out activities
 Encourage the patient to limit activity when fatigue
 Assist the client in planning periods of rest and activity
 Encourage gradual resumption of activities and mild exercise
during recovery.
 PREVENTION AND CONTROL
 Hands should be washed thoroughly after use
of toilet.
 Travelers should avoid water and ice if unsure
to their purity.
 Food handlers should carefully be screened.
 Safe preparation and serving of food must be
practiced.
 The public should be educated on the mode of
transmission of the disease.
 HEPATITIS B
(SERUM HEPATITIS)
 DEFINITION
 Hepatitis B is the inflammation of
the liver caused by Hepatitis B virus.
 Considered to be more serious than
Hepatitis A due to the possibility of
severe complications such as
massive damage and
hepatocarcinoma of the liver.
 ETIOLOGIC AGENT
 Hepatitis b Virus
 The virus has very limited tissue
tropism
 Infects the liver and possibly the
pancreas
 INCUBATION PERIOD

 50 to 189 days or 2 to 5
months with a mean equal to
90 days.
 PERIOD OF COMMUNICABILITY

 The patient is capable of

transmitting the virus during the
later part of the incubation period
and during the acute phase. The
virus may persists in the blood for
many years.
 MODE OF TRANSMISSION
 Person-person contact via infected
body fluids
 Contaminated noodles and syringes
 Infected blood or body fluids
introduced at birth
 Sexual contact
 CLINICAL MANIFESTATIONS
 Prodromal period
 Fever, malaise and anorexia
 Nausea, vomiting, abdominal discomfort,
fever and chills
 Jaundice, dark urine and pale stool
 Recovery is indicated by a decline of fever and
improved appetite
 Fulminant Hepatitis may be fatal and
manifested by severe symptoms like ascitis
and bleeding.
 DIAGNOSTIC PROCEDURES
 Compliment fixation test
 Radio-immunoassay-hemaglutinin test
 Liver function test
 Bile examination in the blood and urine
 Blood count
 Serum transaminase- SGOT, SGPT,ALT
 HbsAg
 PREVENTION
 Blood donors must be screened
 Caution must be observed in giving care
to patients with known HBV
 Hands and other skin areas must be
washed immediately.
 Avoid injury with sharp objects.
 Use disposable needles and syringes
once and discard properly.
 Avoid sharing of toothbrush/ rasor and
other instruments that maybe
contaminated blood.
 Observe safe sex.
 Have adequate rest and sleep and
exercise.
 Eat nutritious food.
 Be vaccinated!
HEPATITIS C
 Rare
 Usually transmitted through blood
transfusion from asymptomatic
donors and by receiving tattoos.
 Associated with high rate of chronic
liver diseases ( chronic hepatitis,
cirrhosis, and increased risk for
hepatocarcinoma)
 Considered INFECTIOUS!
HEPATITIS D
 Found only in patients with acute or
chronic episodes of hepatitis B and
requires presence of HbsAg.
 Depends on the double-shelled type
B virus to replicate.
 Can’t outlast type B infection.
HEPATITIS E
 Transmitted enterically (fecal
-oral and water borne routes)
like hepatitis A.
 Inconsistently in shed in feces,
therefore, detection is difficult.
 SIGNS AND SYMPTOMS
 Prodromal stage
 Easy fatigue, anorexia, body
malaise,headache,arthralgia,myalgia,
photophobia and nausea and vomiting.
 Changes in patients smell and taste.
 There is moderate grade fever (37.8-39.9
C)
 Urine may revealed dark colored and
stool is clay colored.
 Clinical jaundice stage
manifest pruritus, abdominal
pain/tenderness and indigestion
Yellowish discoloration of sclera, mucous
membrane and skin which lasts for 1-2
weeks.
Skin rashes, erythematous patches and
urticaria maybe seen specially when
suffering in HAV and HBV.
Pain, tenderness of right upper quadrant,
enlarged and tender liver, splenomegally
and cervical adenopathy are present.
 Recovery stage
Symptoms decreased or subside
Lasts for 2-12 weeks
 NONVIRAL HEPATITIS
 Classified as toxic or drug
induced( idiosyncratic hepatitis)
 Most of the patients recover in
this type of hepatitis although if
you develop fulminating
hepatitis or cirrhosis.
 CAUSES
 Alcohol overuse
 Direct hepatotoxicity
 Idiosyncratic hepatotoxicity
 Cholestatic reactions
 Metabolic autoimmune disorders
 Infectious agents
 SUMMARY OF DIAGNOSIS
 Hepatitis A: Detection of anti body to hepatitis
A confirms the diagnosis.
 Hepatitis B: Presence of HbsAg and hepatitis B
antibodies confirms the diagnosis.
 Hepatitis C: Depends on the serologic testing
for the specific antibody, one or more months
after the onset of acute hepatitis.
 Hepatitis D: Detection of intrahepatic delta or
immuniglobulin M(IgM) an IgG establishes the
Dx.
 Hepatitis E: Detection of Hepatitis E antigen
supports the diagnosis.