Classification Of Communicable Diseases c1h3e

Communicable disease Communicable diseases spread from one person to another or from an animal to a person. The spread often happens via airborne viruses or bacteria, but also through blood or other bodily fluid. The infectious and contagious are also used to describe communicable disease. In this section, learn about coordinated efforts to combat a few of the most serious communicable diseases on a global level. CLASSIFICATION OF COMMUNICABLE DISEASES A convenient method is to classify communicable diseases according to the mode of transmission. Such classification facilitates the control of these diseases because transmission is the most vulnerable part in the chain of spread. The measures of prevention and control, in general, are similar for diseases in the same group. It is often difficult to tackle the host, i.e. the man. It is again relatively difficult to tackle the causative agent at the source since the source, in most cases is the man himself. In practice, one finds it comparatively easier to attack the agent in the environment in relation to the vehicle of transmission. In this background, communicable diseases are grouped into airborne or respiratory infections, water and food-borne or intestinal infections, or surface infections and arthropod-borne infections.

Mode of transmission 1. Direct droplet transmission: Droplets of sputum from nose and mouth of one person are projected directly on to the conjunctiva or into the nose and mouth of another person in close proximity during the acts of breathing, coughing, talking, laughing, or sneezing. This can happen upto a distance of one meter between two persons and takes place in case of agents having low viability, such as those of common cold and whooping cough. 2. Direct air-borne: Some droplets or droplet nuclei are inhaled with air directly as they remain suspended in the air and are carried by air currents over longer distance. Measles and chickenpox spread in this manner. 3. Indirect air-borne: Some large droplets fall on the clothes, cots or floor and remain there, making them secondary reservoirs of infection. When these droplets dry up, the pathogens are inhaled as such or along with dust during bed-making, dusting and sweeping. The agents may even be carried by air currents and inhaled later. Such transmission occurs in psittacosis, typhus fever, streptococcal sore throat and tuberculosis. 4. transmission: It makes place directly by kissing and indirectly through contaminated food, milk, hands, surgical instruments and other fomites when they are put in the mouth. Examples are streptococcal sore throat and diphtheria.

A. Air-borne Infections:The causative agents produce infection and disease after they are inhaled. The primary pathological process is usually in the respiratory tract. The infection may ultimately manifest as a respiratory disease (e.g. diphtheria, tuberculosis) or as a no respiratory disease (smallpox, measles, leprosy). The air-borne or respiratory infections have four different modes of spread. Air borne or respiratory infections Viral bacterial a. General a. General 1. Common cold 1. Pneumonia 2. Influenza 2. Streptococcal sore throat, acute glomerulonephritis 3. Adenovirus infections and rheumatic fever 4. Viral encephalitis b. Specific* b. Specific 1. Diphtheria 1. Smallpox 2. Whooping cough 2. Chickenpox 3. Tuberculosis 3. Measles 4. Meningococcal meningitis 4. Rubella 5. Mumps

B. Water and Food-borne (Intestinal) Infections:That spread through contamination of water and food. Such contamination is usually fecal in nature. The infecting agent enters the body along with water and food, multiples in intestines and is ed out in stools. When infected stools contaminate water, milk, food, hands or fomites, it leads to further spread of infection. Flies and dust can also provide a link between feces and food. The infecting organism may not have its breeding ground in the intestine, and may not always enter by mouth or leave through anus in case of some worms. Viral Enterovirus infections Infective hepatitis Poliomyelitis

Water and food-borne infections Bacterial Protozoal Cholera Amoebiasis Food poisoning Giardiasis Enteric fever Balantidiasis Brucellosis Diarrhea

Worms Flukes Tapeworms Trichinellosis Threadworm

C. OR SURFACE INFECTIONS The infection comes out of the skin or mucous membrane of the patient and enters through the skin and mucous membrane of a healthy person through bodily or sex . The infection may also be carried indirectly through fomites, such as kajal stick and handkerchief in case of trachoma, towels in case of gonorrheal vulvovaginitis and socks in case of ringworm. D. Arthropod-borne Infections As mechanical carriers: When the infection is carried on the wings, legs, and mouth parts of flies, etc. Food and drinks become infected when flies sit on them. Cholera and some other water and foodborne diseases are spread in this manner. 2. As biological vectors: When the disease agent develops or multiplies in the body of the vector. In many cases, vector is the definitive host while man is the intermediate host. The time ed by the agent in the vector’s body is called ‘extrinsic incubation period’. The vector is not infective during this period The agent may be transferred from arthropod to man by inoculation (e.g. mosquito bite), or by contamination of skin. Such contamination may occur through infective feces of the vector in case of housefly and through infected body fluids in case of louse when it gets crushed on the skin.

The following infections:• Nonspecific viral infections – Common cold – Influenza • Specific viral infections – Smallpox (Variola) – Chickenpox (Varicella) – Measles (Rubeola) – Mumps

– German measles (Rubella) • Nonspecific bacterial infections – Pneumonias – Streptococcal sore throat • Specific bacterial infections – Diphtheria – Whooping cough – Meningococcal meningitis – Tuberculosis. Nonspecific Viral Infections 1. Common Cold (Acute Coryza) Among the acute respiratory illness two-thirds to three fourths are caused by viruses. Most of these viral infections affect the upper respiratory tract, but lower respiratory tract can be involved in certain groups’ particularly in young age group and in certain epidemiological settings. The illness caused by respiratory viruses expressed into multiple distinct syndromes, such as common cold, pharyngitis, croup, tracheobronchitis, bronchiolitis, pneumonia, etc. Almost everybody suffers from common cold sometime in his life. It occurs more in winter and in cold climates. It is an acute infection of the respiratory tract characterized by sneezing, running nose, nasopharyngeal irritation and malaise lasting two to seven days. Fever is rare. The infectious agent is a rhinovirus with more than 100 serotypes. The patient is highly infective 24 hours preceding and five days following the onset of the disease. Transmission is by droplet method or through fomites such as handkerchief. Susceptibility is general. Immunity is shortlived and lasts for a month or so. Incubation period is 12 to 72 (usually 24) hours. There is no specific treatment. Cold vaccines have been used but the results are not encouraging 2. Influenza Influenza is an acute infectious respiratory disease caused by RNA viruses of the family orthomyxoviridae(the influenza viruses). The influenza virus, known to be circulating as a human pathogen since at least the16th century is notable for its unique ability to cause recurrent epidemics and global pandemics. CLINICAL FEATURES Infection with influenza may be asymptomatic but usually gives rise to fever and typical prostrating disease, characteristic in epidemics. Usual symptoms are flushed face, congested

conjunctivae, cough, sore throat, and fever for two to three days, headache, myalgia, back pains and marked weakness. Pneumonia due to secondary bacterial infection is the most common complication CHARACTERISTICS OF INFLUENZA PANDEMICS • Occurrence outside the usual season • Extremely rapid transmission with concurrent outbreaks throughout the globe • High attack rates in all age groups with high mortality rates even in young adults. CAUSATIVE AGENT Influenza viruses are RNA viruses of orthomyxoviridae family. The virus has three distinct genera (types A, B or C) based on antigenic differences of their nucleo and matrix proteins. Influenza A viruses are divided into subtypes based on two proteins on the surface of the Virus: the hemagglutinin (H) and the neuraminidase (N). Influenza B viruses are not categorized into subtypes. Currently among many subtypes of viruses, influenzaA (H1N1) viruses, influenza A (H3N2) viruses, and influenza B viruses are circulating worldwide in human. Epidemics are primarily caused by type A viruses and occasionally by type B in human being. Type C influenza virus has been associated with sporadic cases and minor localized outbreaks. Avian influenza viruses (AIV) belong to type A influenza virus. HOST FACTORS Age and sex: As mentioned earlier, the influenza virus maximally attacks those in the age group 5 to 15 years but no age group or sex is spared. Rates of infection are highest among children Immunity: The antibody to H type of antigen prevents initiation of the infection while that to N antigen prevents virus release and spread The level drops to pre infection level by 8 to 12 months. MODE OF TRANSMISSION Influenza viruses predominantly transmitted through respiratory droplets of coughs and sneezes from an infected person. Influenza viruses may also spread through direct (skin to skin) or indirect with infected material, which ultimately enters through nasopharyngeal route. Transmission of viruses starts one day before the onset of symptoms and continue up to five to seven days after the symptoms subsides. TRANSMISSION OF INFLUENZA VIRUSES FROM

ANIMALS TO PEOPLE Influenza A viruses are found in many different animals, including ducks, chickens, pigs, whales, horses and seals. Wild birds are the primary natural reservoir for all subtypes of influenza A viruses and are thought to be the source of influenza A viruses in all other animals. Pigs can be infected with human, avian and swine influenza viruses and there is possibility of development of new strain due to genetic reassortment among the viruses of different species. Incubation Period The incubation time for influenza ranges from one to five days with an average of two days. Diagnosis Traditionally, the definitive diagnosis of influenza is made either on the basis of virus isolation or by serology • Detection of antigen in nasal secretions by: – Rapid test: It can be used to detect influenza viruses within 30 minutes. – Immunofluorescence test – Antigen capture ELISA with monoclonal antibody to the nucleoprotein – Reverse Transcriptase Polymerase Chain Reaction (RT-PCR) • Virus isolation: – Cell line Madin-Darby Canine Kidney cells (MDCK) – Egg inoculation • Serological test in paired serum samples

CONTROL OF INFLUENZA Influenza vaccination is the key strategy for the prevention of influenza during the interpandemic periods and a pillar of pandemic preparedness. Antiviral drugs can only be used as an adjunct. Resistant mutants of both the classes of antiviral agents have been detected. WHO RECOMMENDS THE FOLLOWING PRIORITY CASES FOR VACCINATION • Elderly non institutionalized individuals suffering from chronic conditions such as Pulmonary or Cardiovascular disease, metabolic illness including diabetes mellitus and renal dysfunction, various types of immunosuppressant including persons with AIDS and transplant recipients.

• All adults and children aged over six months suffering from any of the conditions mentioned above. • Health care persons in regular and frequent with high risk persons. • Household s of high-risk persons including elderly and the disabled. • Pregnant women who will be in their second or third trimester by the start of the influenza season. Treatment: 1. Antibiotics for bacterial complications of influenza 2. Antiviral therapy 3. Management of s may include-antiviral prophylaxis and advice about relevant vaccination (e.g. pandemic strain vaccine if available). Prevention and control strategies: People with respiratory infection symptoms should practice the following respiratory etiquette. All symptomatic people should: 1. Avoid close (less than 1 meter) with other people. 2. Cover their nose and mouth when coughing or sneezing. 3. Use disposable tissues to contain respiratory secretions. 4. Immediately dispose off used tissues. Social distancing: 1. Crowded places and large gatherings of people should be avoided at the time of an influenza pandemic, whether such gatherings are open or closed spaces. 2. A distance of at least 1 meter should be maintained between persons wherever possible 3. Any form of with people who are unwell with pandemic influenza, including visitors, should be avoided wherever practicable. 4. Movement of people in and out of the area will be effectively restricted to prevent further spread to unaffected areas

RECOMMENDED DRUGS AND DOSAGE FOR PROPHYLAXIS OF INFLUENZA • Amantadine 5 mg/kg/day up 5 mg/kg/day

• Rimantadine • Oseltamivir • Zanamivir Specific Viral Infections I.

Smallpox (Variola) Smallpox has been one of the greatest scourges and a major killer of mankind. Till the discovery of vaccination, smallpox was responsible for the death of one out of every five children below five years of age. In October 1979, the WHO certified that smallpox had been eradicated from the world. This was confirmed by the World Health Assembly on 8th May 1980

Fig 1 small pox CLINICAL FEATURES Differences between smallpox and chickenpox Characteristics Smallpox Chickenpox Incubation period 7-17 days, average 12 7-12 days, average 15 Fever For 2-3 days at the onset and One day at the onset rising with again when pustules appear. each fresh crop of lesions Prodromal symptoms Rash • Distribution Appearance and progress • Lesions • Evolution Sequelae

Severe First on periphery and then towards center, (centrifugal) Appears on 3rd day and progresses in stages Shotty, deep seated, multilocular Pustules 1 cm or more in size Slow, deliberate and majestic Disfiguration, blindness and death

Mild First on trunk and then towards periphery, (centripetal) Appears on 1st day and comes in crops Superficial, unilocular, surrounded Small, elliptical, mostly discrete; Very rapid Residual sequelae rare. Leaves only pink stains but not permanent or pitted

Leaves pitted scars

scars

LABORATORY DIAGNOSIS: This is confirmed by: • Tissue culture • Serological examination • Electron microscopy This is now eradicated world wide. II.

Chickenpox (Varicella) (ICD-B01.9) CLINICAL PICTURE Chickenpox is important because it is mistaken with a more dangerous disease, i.e. modified smallpox. Symptoms and signs of the two have already been compared. Chickenpox is a mild disease but varies in intensity. There may be just one to two pocks or the disease may take serious and fatal, though rare, forms such as varicella bullosa, v. gangrenosa and v. hemorrhagica. Encephalitis and pneumonia are rare complications.

Fig 2 chicken pox

Types of chickenpox a) Breakthrough Varicella In previously immunized children asymptomatic infection with wild type of virus may occur. When a child develops rash after 42 days of chickenpox vaccination and is due to wild type of Varicella-Zoster virus, is known as breakthrough varicella. This breakthrough varicella should be isolated, since they are infectious.

b) Progressive Varicella Progressive varicella is one of the worst complications of primary Varicella-Zoster virus infection, characterized by severe hemorrhage, coagulopathy and continued development of lesions. Immunocompromised children, pregnant women and newborns are most susceptible c) Congenital Varicella Syndrome Congenital Varicella Syndrome develops among two percent of fetuses whose mothers had varicella within first 20 weeks of pregnancy. Limb development is hampered when fetus is infected at 6 to 12 weeks of gestation. Eye and brain development is interrupted, when infection at 16 to 20 weeks of gestation. Horner syndrome and dysfunction of the urethral or anal sphincters may be developed due to viral damage of the sympathetic fibers in the cervical and lumbosacral cord.

DIAGNOSIS • Clinical • Blood – At first leucopenia for first 72 hours; followed by a relative and absolute lymphocytosis. – VZV immunoglobulin G (IgG) antibodies can be detected by several methods and a 4-fold rise in IgG antibodies is also confirmatory of acute infection. CSF: Mild lymphocytic pleocytosis and increase in protein in the cerebrospinal fluid; glucose concentration being normal. • Direct fluorescence assay (DFA) from skin lesions, polymerase chain reaction (PCR) and Tzanck smear or Calcofluor stain to detect multinucleated giant cells.

TREATMENT 1. Oral therapy with acyclovir (20 mg/kg/dose; maximum: 800 mg/dose) given as four doses per day for five days is the drug of choice. In healthy adults, acyclovir 800 mg is given five times a day orally for five days. 2. Immunocompromised patients benefit from both symptomatic and antiviral therapy. Oral acyclovir istered late in the incubation period may modify subsequent varicella in the

normal child. However, its use in this manner is not recommended until it can be further evaluated. When acyclovir resistance is seen then foscarnet is used COMPLICATIONS The complications are more commonly seen in immunocompromised patients. These are 1. Mild thrombocytopenia, purpura, hemorrhagic vesicles, hematuria and gastrointestinal bleeding. Cerebellar ataxia, encephalitis, pneumonia, 2. nephritis, nephritic syndrome, hemolytic-uremic syndrome, 3. arthritis, myocarditis, pericarditis, 4. pancreatitis, and orchitis. 5. Secondary bacterial infections, with group A—hemolytic streptococci and Staphylococcus aureus, are common. 6. Cellulitis, erysipelas, osteomyelitis, and rarely meningitis are observed. Pitted scars are frequent sequelae. 7. Among AIDS patients Varicella-Zoster virus causes acute retinal necrosis and progressive outer retinal necrosis

PREVENTION ive Immunization a) Varicella-zoster immune globulin (VZIG) post exposure prophylaxis is recommended for immunocompromised children, pregnant women, and newborns exposed to maternal varicella. Close between a susceptible high-risk patient and a patient with herpes zoster is also an indication for VZIG prophylaxis.3 If available, b) Varicella-Zoster immunoglobulin (VZIG) in a dose of 15 to 20 units/kg body weight should be istered as a 16.5 percent solution by intramuscular route within 72 hours of exposure, when it is effective in preventing the disease or modifying it.7,8 If it is not available, human c) Immunoglobulin (IG) given promptly in a dose of 0.6to 1.2 ml/kg of body weight may also be effective. Active Immunization a) Vaccine given to normal children within three to five days exposure is effective in preventing or modifying varicella. Varicella vaccine is now recommended for post exposure use, for outbreak control. Live virus vaccine is recommended for routine istration in children at 12 to 18 months of age.10 Children 12 months to 12 years receive a single vaccine dose; adolescents and adults require two vaccine doses, a minimum of four weeks apart.11 Tetravalent combined measles, mumps, rubella, and varicella vaccine (MMRV)has also been investigated.

b) Contraindications: Children with cell-mediated immune deficiencies. Interactions: Varicella vaccine if given within four weeks of MMR vaccine is associated with a higher risk of breakthrough disease; therefore, it is recommended that the vaccines either be istered simultaneously at different sites or be given at least four weeks apart. IAP has recommended varicella vaccine to children only after one to one discussion with parents. c) The potential danger of such vaccination is a latent infection with herpes zoster in later life. III.

RUBEOLA (MEASLES) A. Description 1. Agent: Paramyxovirus 2. Incubation period: 10 to 20 days 3. Communicable period: From 4 days before to 5 days after rash appears, mainly during prodromal stage (pertaining to early symptoms that may mark the onset of disease) 4. Source: Respiratory tract secretions, blood, or urine of infected person 5. Transmission: Airborne particles or direct with infectious droplets; transplacental B. Assessment 1. Fever 2. Malaise 3. The three “C’s”—coryza, cough, conjunctivitis 4. Rash appears as red, erythematous maculopapular eruption starting on the face and spreading downward to the feet; blanches easily with pressure and gradually turns a brownish color (lasts 6 to 7 days); may have desquamation

Fig 3 Measels

5. Koplik’s spots: Small red spots with a bluish white center and a red base; located on the buccalmucosa and last 3 days

Laboratory confirmed measles: A case that meets the clinical case definition and presence of measles specific IgM antibodies in the serum, or at least fourfold increase in antibody titer or isolation of measles virus. COMPLICATIONS 1. 2. 3. 4. 5. 6.

otitis media (5–15%) Pneumonia (5–10%). Bleeding from skin and mucosa may occur (Black measles). Encephalitis subacute sclerosing panencephalitis (SSPE) Malnutrition

Case Management of Measles Case management depends upon severity of disease. Uncomplicated measles: Child with measles and absence of signs and symptoms of complicated or severe disease. This children requires ive measures like 1. Vitamin A oil is given to all children, 2. Breastfeeding is continued along with complementary feeding or fluids as usual, green leafy vegetables, yellow fruits, etc. 3. ORS given in case of diarrhea, fever is treated with paracetamol to reduce risk of convulsion. Complicated measles: Same as mentioned in uncomplicated measles. In addition eye lesions are cleaned and treated with one percent tetracycline eye ointment three times a day for seven days. Ear discharges are cleaned and treated with antibiotics. Pneumonia is also treated. The patient is referred to a health facility for further management C. Interventions 1. Use airborne droplet precautions if the child is hospitalized. 2. Restrict child to quiet activities and bedrest. 3. Use a cool mist vaporizer for cough and coryza. 4. Dim lights if photophobia is present. 5. ister antipyretics for fever. Rationale of giving at nine months of age: Measles vaccine interacts with maternally derived antibody in infants. This antibody persists in the infants till four to six months of age in same quantity from birth. Afterwards it starts

declining gradually from six months till it completely disappears by 15 months. But epidemiologically it has been seen that incidence of measles is more common during nine to ten months of age. That is why it is a satisfactorily compromise between 6 and 15 months of age, i.e. nine months. Measles vaccine can be given earlier after six months of age during an epidemic, or exposure to a case of measles or if the child is malnourished. In that case the vaccine should be repeated again at completion of nine months for better seroconversion, keeping a minimum gap of four weeks. If the child comes late, then this vaccine can be given till five years of age. IV.

ROSEOLA (EXANTHEMA SUBITUM)

A. Description 1. Agent: Human herpesvirus type 6 2. Incubation period: 5 to 15 days 3. Communicable period: Unknown, but thought to extend from the febrile stage to the time the rash first appears 4. Source: Unknown 5. Transmission: Unknown Assessment 1. Sudden high (>38.8 C [>102 F]) fever of 3 to 5 days’ duration in a child who appears well, followed by a rash (rose-pink macules that blanch with pressure) 2. Rash appears several hours to 2 days after the fever subsides and lasts 1 to 2 days. C. Interventions: ive V.

RUBELLA (GERMAN MEASLES)

A. Description 1. Agent: Rubella virus 2. Incubation period: 14 to 21 days 3. Communicable period: From 7 days before to about 5 days after rash appears 4. Source: Nasopharyngeal secretions; virus is also present in blood, stool, and urine 5. Transmission a. Airborne or direct with infectious droplets

b. Indirectly via articles freshly contaminated with nasopharyngeal secretions, feces, or urine c. Transplacental B. Assessment 1. Low-grade fever 2. Malaise 3. Pinkish red maculopapular rash that begins on the face and spreads to the entire body within 1 to 3 days

Fig 4 German Measels 4. Petechial red, pinpoint spots may occur on the soft palate. 5. lymphadenopathy Clinical manifestations of Congenital Rubella General  Fetal loss (spontaneous abortion and stillbirths)  Low birth weight  Micrognathia Ears and central nervous system  Sensorineural deafness: unilateral or bilateral  Central auditory deafness  Mental retardation,  Speech defects, Autism Cardiovascular system  Patent ductus arteriosus (PDA)  Pulmonary arterial stenosis  Ventricular septal defects Eyes 

Retinopathy

 Cataracts: pearly, dense, nuclear; 50 percent bilateral  Microphthalmos Transient neonatal manifestations  Thrombocytopenia, +/- purpura  Hepatospenomegaly  Meningoencephalitis  Bony radiolucencies  Adenopathies Late-emerging or developmental  Late-onset interstitial pneumonitis, 3-12 months  Chronic diarrhea  Insulin-dependent diabetes mellitus (type I)  Thyroiditis

Fig 5 pathophysiology C. Interventions 1. Use airborne droplet precautions if the child is hospitalized; provide ive treatment. 2. Isolate the infected child from pregnant women. Prevention:1. rubella vaccines 2. If a woman in early pregnancy is found to have ed rubella, medical termination of pregnancy is indicated. The occurrence of such infection may or may not be clinically

evident. Confirmation can be obtained through serological tests and through isolation of the virus.7 • Serological tests – Presence of rubella specific IgM indicative of recent infection. – Four-fold rise in antibody titer over two serum samples collected 7 to 14 days apart, the first sample being taken as soon as possible (within ten days of onset of suspected illness). • Isolation of virus 3. Antenatal infection of the fetus can be confirmed in the newborn by the presence of specific IgM antibodies in the serum. VI.

MUMPS A. Description 1. Agent: Paramyxovirus 2. Incubation period: 14 to 21 days 3. Communicable period: Immediately before and after parotid gland swelling begins 4. Source: Saliva of infected person and possibly urine 5. Transmission: Direct or droplet spread from an infected person

Assessment 1. Fever 2. Headache and malaise 3. Anorexia 4. Jaw or ear pain aggravated by chewing, followed by parotid glandular swelling 5. Orchitis may occur

Pathophysiology 1. Initial features are swelling of parotid gland obliterating the sulcus behind the ear lobule; fever 37.8 to 38.3°C for a day or so; and pain and tenderness in masseter region. 2. One and two days later, other parotid or salivary glands may become involved. The degree of swelling, pain or discomfort may vary. 3. This usually reaches its peak about two days after the onset and subsides between four to seven days. The parotid swelling extends from tip of the mastoid over the ramus of

mandibule forward to the cheek and downwards towards the neck, thus obliterating the space between tip of the mastoid and angle of the mandibule. 4. Inability to feel the tip of the mastoid aids in differentiating between parotis and cervical adenitis. During its prodrome, cowie’s sign first appears that is swelling and outpouching of the openings of stensten’s duct on the buccal mucosa opposite the third upper molar. 5. Similarly the orifices of sublingual and submaxillary glands become swollen and edematous. Leukocytosis occurs with an increase in lymphocytes. 6. Virus may be found in saliva, blood and cerebrospinal fluid.

Fig 6 mumps C. Interventions 1. Institute airborne droplet precautions. 2. Provide bedrest until the parotid gland swelling subsides. 3. Avoid foods that require chewing. 4. Apply hot or cold compresses as prescribed to the neck. 5. Apply warmth and local with snugfitting underpants to relieve orchitis. PREVENTION 1. Live mumps vaccines are available as monovalent mumps vaccine, bivalent measles– mumps (MM) vaccine, and trivalent measles–mumps–rubella (MMR) vaccine. 2. Sorbitol and hydrolysed gelatin are used as stabilizers in mumps vaccine, and neomycin is added as a preservative. 3. Once reconstituted, live attenuated mumps vaccines must be used immediately or stored at 0 to 8°C, kept away from light, and discarded if not used within eight hours. 4. Vaccine may be istered 0.5 ml intramuscularly after one year of age. There are very few contraindications to mumps vaccination. 5. Mumps vaccine should not be istered to individuals with immune deficiency or immunosuppression; Complication:-

1. 2. 3. 4. 5. 6.

Oophoritis and mastitis may occur in females; very rarely pancreatitis Insulin dependent diabetes mellitus may occur Aseptic meningitis central nervous system is frequently infected Meningitis5 and deafness6 are well recognized complication of mumps. Transient electrocardiogram abnormalities, mainly changes in T waves and ST segments, have been reported in up to 15 percent of cases; while rare case reports of fatal nephritis or myocarditis have been published

Specific Bacterial Infections I.

PERTUSSIS (WHOOPING COUGH) A. Description 1. Agent: Bordetella pertussis 2. Incubation period: 5 to 21 days (usually 10 days) 3. Communicable period: Greatest during the catarrhal stage (when discharge from respiratory secretions occurs) 4. Source: Discharge from the respiratory tract of the infected person 5. Transmission: Direct or droplet spread from infected person; indirect with freshly contaminated articles B. Assessment 1. Symptoms of respiratory infection followed by increased severity of cough, with a loud whooping inspiration 2. May experience cyanosis, respiratory distress, and tongue protrusion 3. Listlessness, irritability, anorexia  



Catarrhal stage: It lasts for five to ten days. The child has mild fever and catarrh with irritating cough which is worse at night. Paroxysmal stage: This is characterized by bouts or paroxysms of cough. During each bout, the child coughs five to ten times in rapid succession followed by holding of breath, stimulation of respiratory center and forced inspiration associated with a whooping sound. This restores color and strength to the child exhausted by the bout of cough. The child may experience five to ten paroxysms per day. The child may urine or stools during an attack of cough and may bite his tongue. Whooping cough may be complicated by occurrence of hernia, rectal prolapsed and superadded pulmonary infection. The paroxysmal stage may last for up to six weeks. Convalescent stage: It lasts for 1–2 weeks.

Fig 6 Pertusis pathogenesis Confirmed (Laboratory Tests) Isolation of Bordetella pertussis or detection of genomic sequences by means of the polymerase chain reaction (PCR) or Positive paired serology. DIAGNOSIS It depends upon the recovery of the causative organism from nasopharyngeal swab obtained during the catarrhal and early paroxysmal stages. C. Interventions a. Isolate child during the catarrhal stage; if the child is hospitalized, institute airborne droplet precautions. b. ister antimicrobial therapy as prescribed.

c. Reduce environmental factors that cause coughing spasms, such as dust, smoke, and sudden changes in temperature. d. Ensure adequate hydration and nutrition. e. Provide suction and humidified oxygen if needed. f. Monitor cardiopulmonary status (via monitor as prescribed) and pulse oximetry. g. Infants do not receive maternal immunity h. VACCINATION II.

DIPHTHERIA A. Description 1. Agent: Corynebacterium diphtheriae 2. Incubation period: 2 to 5 days 3. Communicable period: Variable, until virulent bacilli are no longer present (three negative cultures of discharge from the nose and nasopharynx, skin, and other lesions); usually 2 weeks, but can be 4 weeks 4. Source: Discharge from the mucous membrane of the nose and nasopharynx, skin, and other lesions of the infected person 5. Transmission: Direct with infected person, carrier, or contaminated articles The following WHO defined clinical conditions are associated with increasing risk of toxininduced systemic disease: a. The catarrhal form (erythema of pharynx, no membranes), b. The follicular form (patches of exudates over pharynx and the tonsils), c. The spreading form (membranes covering the tonsils and posterior pharynx), and d. The combined form (more than one anatomical site involved, for example throat and skin)

Fig 7 Diphtheria pseudo membrane changes DIAGNOSIS

During outbreaks, clinical diagnosis is based on typical pseudo membraneous pharyngitis. Although laboratory investigation of suspected cases is strongly recommended, treatment should not be delayed while waiting for the laboratory results. Bacterial culture is the mainstay of etiological diagnosis. Schick test It is done by giving 0.2 ml (1/50 MLD) of Schick test antigen or toxin intradermally in one forearm, and heated toxin in the other for control. As an alternative, 0.1 ml fluid diphtheria toxoid vaccine in 1:10 dilution may be injected intradermally.7 The arms are inspected at 24 to 48 hours. The test is interpreted as follows: • No reaction on either arm—Negative reaction. The person tested has enough antitoxin (0.03 units per ml serum) to neutralize the antigen. • Test arm develops a circumscribed red flush, 1 to 5 cm in diameter, at 24 to 48 hours while the control arm does not show any reaction—Positive reaction. The flush is most marked on the fourth day. It then fades, becomes brown and desquamates on 5th to 7th day. A person with positive reaction is susceptible to diphtheria and needs immunization. • Both arms develop an equal flush, less circumscribed than in a positive case—False positive reaction. The flush fades quickly and disappears by fourth day. This occurs due to allergic reaction to the foreign protein in the toxin. The test is read as negative and indicates adequate immunity. • Test arm shows true positive reaction and control arm shows false positive reaction— Combined reaction. Such a person is susceptible to diphtheria as well as allergic to the antigen. He should be vaccinated cautiously, using very small but multiple doses.

B. Assessment Low-grade fever, malaise, sore throat, Dense pseudo membrane formation of the throat that may interfere with eating, drinking, and breathing. 1. Lymphadenitis, neck edema, “bull neck” 2. Faucial: It is characterized by fever ranging from 37.8 to 38.3°C, rapid pulse, enlarged cervical glands and spots of exudate or false membrane on the pillars of fauces, tonsils or pharynx. There may be bleeding if the membrane is detached. There is little or no pain in the throat. High fever 39.4 to 40°C is uncommon in diphtheria and is more suggestive of streptococcal infection. Fatality varies from 2 to 14 percent. 3. Laryngeal: It may be primary or secondary to faucial diphtheria and is characterized by hoarseness, loss of voice, croupy cough, and obstruction to breathing and regression of chest wall, respiratory failure and death. Infection may spread to trachea. It is the most fatal form.

4. Anterior nasal: It is characterized by blood stained nasal discharge and ulcers on the nose, upper lip and cheek. It is a less toxic form of diphtheria. 5. Other forms: These are conjunctival and cutaneous diphtheria in which the membrane forms on ulcers or wounds. Membranous vulvovaginitis may occur in children through common towels used in the nursery C. Interventions 1. Ensure strict isolation for the hospitalized child. 2. ister diphtheria antitoxin as prescribed (after a skin or conjunctival test to rule out sensitivity to horse serum). 3. Provide bedrest. 4. ister antibiotics as prescribed. 5. Provide suction and humidified oxygen as needed. 6. Provide tracheostomy care if a tracheostomy is necessary.. Foul-smelling, mucopurulent nasal discharge III.

TUBERCULOSIS A. Description 1. Tuberculosis is a contagious disease caused by Mycobacterium tuberculosis, an acid-fast bacillus 2. Multidrug-resistant strains of M. tuberculosis occur because of child or family noncompliance with therapeutic regimens. 3. The route of transmission of M. tuberculosis is through inhalation of droplets from an individual with active tuberculosis. 4. There is an increased incidence in urban lowincome areas, nonwhite racial or ethnic groups, and first-generation immigrants from endemic countries. 5. Most children are infected by a family member or by another individual with whom they have frequent , such as a babysitter. INCUBATION PERIOD It is 4 to 12 weeks from infection to primary lesion, but from infection to disease it may be years. The chances of getting the disease are more during first 6 to 24 months of life. HOST FACTORS:

Heredity: It plays little role, if any, as a determinant of tubercular infection.

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Race: Caucasian (which includes most Indians) and Mongoloid races have a distinct natural resistance to tuberculosis compared to Africans, American Indians and Eskimos. Age: Children under two are most susceptible to new infection. The resistance starts increasing at two years and is high in school age, i.e. 5 to 12 years Sex: Prevalence of tubercular disease is higher in males than in females at all ages Malnutrition: Extreme malnutrition or general debility would certainly make a person more prone to tuberculosis or any other infective disease. Specific immunity: It is acquired through primary subclinical infection or BCG vaccination and provides Good protection against the disease. The immunity is mainly cell mediated in nature, operating largely through T lymphocytes. The role of immunoglobulins is less clear, though it is known that serum IgA is often increased in patients with active tuberculosis and drops as the infection is controlled by therapy. Immunity should not be confused with tuberculin hypersensitivity, which is the reaction to tuberculin, a protein derivative of the broth in which tuberculin bacilli have been grown. Presence of tuberculin hypersensitivity indicates the presence of living tubercle bacilli. The larger the skin reaction, the higher the possibility that the infection is clinically significant.

Environment Factors  Housing: Chances of repeated and massive doses of infection are more when people live in dark, illventilated, overcrowded houses. As a result, the risk of developing tuberculosis is increased.  Social factors: Transmission of tuberculosis is favored by large family size, poverty, ignorance about the mode of spread and occupational environment B. Assessment 1. Child may be asymptomatic or develop symptoms such as malaise, fever, cough, weight loss, anorexia, and lymphadenopathy. 2. Specific symptoms related to the site of infection, such as the lungs, brain, or bone, may be present. 3. With increased time, asymmetrical expansion of the lungs, decreased breath sounds, crackles, and dullness to percussion develop. PATHOGENESIS 1. The characteristic lesion is the tubercle, a nodular collection of epitheliod cells, giant cells and tubercle bacilli in the center, surrounded by lymphocytes and fibroblasts. 2. Adjacent tubercles enlarge and coalesce to form a mass. 3. There is central necrosis, caseation, tissue destruction and peripheral spread. Healing takes place by fibrosis and calcification. 4. Destruction and healing frequently coexist.

Fig 8 Tuberculosis Pathogenesis C. Mantoux test 1. The test produces a positive reaction 2 to 10 weeks after the initial infection. 2. The test determines whether a child has been infected and has developed sensitivity to the protein of the tubercle bacillus; a positive reaction does not confirm the presence of active disease (exposure versus presence). 3. After a child reacts positively, the child will always react positively; a positive reaction in a previously negative child indicates that the child has been infected since the last test. 4. Tuberculosis testing should not be done at the same time as measles immunization (viral interference from the measles vaccine may cause a false-negative result). Mantoux test Interpretation 1. Induration measuring 15 mm or more is considered to be a positive reaction in children 4 years or older who do not have any risk factors. 2. Induration measuring 10 mm or more is considered to be a positive reaction in children younger than 4 years and in children with chronic illness or at high risk for exposure to tuberculosis. 3. Induration measuring 5 mm or more is considered to be positive for the highest risk groups, such as children with immunosuppressive conditions or human immunodeficiency virus infection. Diagnostic evaluation 1. A definitive diagnosis is made by showing the presence of mycobacteria in a culture. 2. Chest x-rays are supplemental to sputum cultures and are not definitive alone. 3. Because an infant or young child often swallows sputum rather than expectorates it, gastric washings (aspiration of lavaged contents from the fasting stomach) may be done to obtain a specimen; the specimen is obtained in the early morning before breakfast.

E. Interventions 1. Medications a. A 9-month course of isoniazid (INH) may be prescribed to prevent a latent infection from progressing to clinically active tuberculosis and to prevent initial infection in children in highrisk situations; a 12-month course may be prescribed for a child infected with human immunodeficiency virus (HIV). b. Recommendation for a child with clinically active tuberculosis may include combination istration of isoniazid, rifampin (Rifadin), and pyrazinamide daily for 2 months, and then isoniazid and rifampin twice weekly for 4 months. c. Inform the parents and child that bodily fluids including urine may turn an orange-red color with some tuberculosis medications. Directly observed therapy may be necessary for some children. 2. Place children with active disease who are contagious on respiratory isolation until medications have been initiated, sputum cultures show a diminished number of organisms, and cough is improving; this includes use of a personally fitted air-purifying N95 or N100 respirator (mask) by the nurse caring for the child. 3. Stress the importance of adequate rest and adequate diet. 4. Instruct the child and family about measures to prevent the transmission of tuberculosis. 5. Case finding and follow-up with known s is crucial to decrease the number of cases of individuals with active tuberculosis. IV. HEPATITIS Description: An acute or chronic inflammation of the liver that may be caused by a virus, a medication reaction, or another disease process.

Fig 9 Hepatitis changes in liver

A. Hepatitis A (HAV) 1. Highest incidence of HAV infection occurs among preschool or school-age children younger than 15 years. 2. Many infected children are asymptomatic, but mild nausea, vomiting, and diarrhea may occur. 3. Infected children who are asymptomatic still can spread HAV to others. B. Hepatitis B (HBV) 1. Most HBV infection in children is acquired perinatally. 2. Newborn infants are at risk if the mother is infected with HBV or was a carrier of HBV during pregnancy. 3. Possible routes of maternal-fetal (infant) transmission include leakage of the virus across the placenta late in pregnancy or during labor, ingestion of amniotic fluid or maternal blood, and breast-feeding, especially if the mother has cracked nipples. 4. The severity in the infant varies from no liver disease to fulminant (severe acute course) or chronic active disease. 5. In children and adolescents, HBV occurs in specific high-risk groups, including children with hemophilia or other disorders requiring multiple blood transfusions, children or adolescents involved in IV drug abuse, institutionalized children, preschool children in endemic areas, and children who have had heterosexual activity or sexual activity with homosexual men. 6. Infection with HBV can cause a carrier state and lead to eventual cirrhosis or hepatocellular carcinoma in adulthood. C. Hepatitis C (HCV) 1. Transmission of HCV is primarily by the parenteral route. 2. Some children may be asymptomatic, but HCV often becomes a chronic condition and can cause cirrhosis and hepatocellular carcinoma. D. Hepatitis D 1. Infection occurs in children already infected with HBV. 2. Acute and chronic forms tend to be more severe than HBV and can lead to cirrhosis. 3. Children with hemophilia are more likely to be infected, as are children who are IV drug s. E. Hepatitis E 1. Infection is uncommon in children. 2. Infection is not a chronic condition, does not cause chronic liver disease, and has no carrier state. F. Hepatitis G 1. Hepatitis G virus is blood-borne and is similar to HCV. 2. High-risk groups include transfusion recipients, IV drug s, and individuals infected with HCV. 3. Individuals are often asymptomatic, and most infections are chronic.

Assessment a) Prodromal or Anicteric Phase Lasts 5 to 7 days Absence of jaundice Anorexia, malaise, lethargy, easy fatigability Fever (especially in adolescents) Nausea and vomiting Epigastric or right upper quadrant abdominal pain Arthralgia and rashes (more likely with hepatitis B virus) Hepatomegaly b) Icteric Phase Jaundice, which is best assessed in the sclera, nail beds, and mucous membranes Dark urine and pale stools Pruritus Prevention  Immunoglobulin provides ive immunity and may be effective for pre-exposure prophylaxis to prevent HAV infection.  Hepatitis B immunoglobulin provides ive immunity and may be effective in preventing infection after a one-time exposure (should be given immediately after exposure), such as an accidental needle puncture or other of contaminated material with mucous membranes; immunoglobulin should also be given to newborns whose mothers are positive for hepatitis B surface antigen.  Hepatitis A vaccine and hepatitis B vaccine:  Proper hand washing and standard precautions can prevent the spread of viral hepatitis. Interventions  Strict hand washing is required.  Hospitalization is required in the event of coagulopathy or fulminant hepatitis.  Standard precautions and enteric precautions are followed during hospitalization.  Provide enteric precautions for at least 1 week after the onset of jaundice with HAV.  The hospitalized child usually is not isolated in a separate room unless he or she is focally incontinent and items are likely to become contaminated with feces.  Children are discouraged from sharing toys.  Instruct the child and parents in effective hand washing techniques.  Instruct the parents to disinfect diaper-changing surfaces thoroughly with a solution of 1/4 cup bleach in 1 gallon of water.  Maintain comfort, and provide adequate rest and sleep.  Provide a low-fat, well-balanced diet.  Inform the parents that because HAV is not infectious 1 week after the onset of jaundice, the child may return to school at that time if he or she feels well enough.

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V.

Inform the parents that jaundice may appear worse before it resolves. Caution the parents about istering any medications to the child; explain the role of the liver in detoxification and excretion of medications in understandable . Instruct the parents about the signs of the child’s condition worsening, such as changes in neurological,status, bleeding, and fluid retention.

POLIOMYELITIS

A. Description 1. Agent: Enteroviruses 2. Incubation period: 7 to 14 days 3. Communicable period: Unknown; the virus is present in the throat and feces shortly after infection and persists for about 1 week in the throat and 4 to 6 weeks in the feces 4. Source: Oropharyngeal secretions and feces of the infected person 5. Transmission: Direct with infected person; fecal-oral and oropharyngeal routes B. Assessment 1. Fever, malaise, anorexia, nausea, headache, sore throat 2. Abdominal pain followed by soreness and stiffness of the trunk, neck, and limbs that may progress to central nervous system paralysis

Fig 10 poliomyelitis changes

CLINICAL ASPECTS 1. Abortive polio: Occurs in 4 to 8 percent of infections and is characterized by minor illness with low grade fever, malaise, sore throat, vomiting, abdominal pain, and loss of appetite. Recovery is rapid and complete, there is no paralysis. It cannot be distinguished from other viral infections causing mild respiratory tract or gastrointestinal infections. 2. Nonparalytic aseptic meningitis: Occurs in 1 to 2 percent of infections and is characterized by headache, neck, back and leg stiffness several days after a prodrome similar to abortive polio. Cases recover within 2 to 10 days. It cannot be distinguished from other causes of aseptic meningitis. Illness may reach imminent paralysis but soon reverts back. 3. Paralytic poliomyelitis: Occurs in 0.5 to 1 percent of infections. Symptoms often occur in two phases, minor and major and are often separated by several days without symptoms. Minor phase consists of symptoms similar to those of abortive poliomyelitis. The major phase of illness begins with muscle pain, spasms and the return of fever. This is followed by rapid onset of flaccid paralysis that is usually complete within 72 hours. a. Spinal form: This is probably the most common form of paralytic muscles is asymmetrical and the extent of paralysis is variable. Paralytic manifestation in extremities begin proximally and progress to involve distal muscle groups b.Bulbar and bulbospinal forms: These for only 10 percent cases of paralytic poliomyelitis and are usually life threatening. Pure bulbar form is rare. Pure bulbar form is rare and results from a cranial nerve lesion, resulting in respiratory insufficiency and difficulty in swallowing, eating or speaking. c. Encephalitic form: The child may be irritable, delirious, disoriented or stuperose and may have convulsions. C. Interventions 1. Enteric precautions 2. ive treatment 3. Bedrest 4. Monitoring for respiratory paralysis 5. Physical therapy

TREATMENT OF PARALYTIC POLIOMYELITIS a. Complete bed rest in; comfortable but rotating positions should be maintained in a “polio bed”: firm mattress, footboard, sponge rubber pads or rolls, sandbags, and light splints, massage or intramuscular injection is contraindicated during the acute phase b. Correct positioning of affected limbs,

c. d. e. f. g.

ive movements and physiotherapy of the ts after the acute phase subsides, Warm water fomentation, Symptomatic treatment for fever and pain, Have to report immediately if there is progression of paralysis and Orthopedic surgery for deformities or contractures.

STRATEGIES FOR POLIO ERADICATION • Routine immunization: This is carried out as per national Immunization Schedule. • Supplementary immunization activity (SIA): – NID (National Immunization Day): the entire country is covered with OPV. – SNID ( Sub National Immunization Day): some states or parts of states are covered. – Mop up immunization: final end game strategy; when wild virus transmission is very much focal • Surveillance of acute flaccid paralysis (AFP): This is done to identify areas of wild polio virus transmission and to guide immunization activities accordingly SCARLET FEVER A. Description 1. Agent: Group A beta-hemolytic streptococci 2. Incubation period: 1 to 7 days 3. Communicable period: About 10 days during the incubation period and clinical illness; during the first 2 weeks of the carrier stage, although may persist for months 4. Source: Nasopharyngeal secretions of infected person and carriers 5. Transmission: Direct with infected person or droplet spread; indirectly by with contaminated articles, ingestion of contaminated milk, or other foods Assessment 1. Abrupt high fever, flushed cheeks, vomiting, headache, enlarged lymph nodes in the neck, malaise, abdominal pain 2. A red, fine sandpaper-like rash develops in theaxilla, groin, and neck that spread to cover the entire body except the face. 3. Rash blanches with pressure (Schultz-Charlton reaction) except in areas of deep creases and folds of the ts (Pastia’s sign). 4. Desquamation, sheet-like sloughing of the skin on palms and soles, appears by weeks 1 to 3.

5. The tongue is initially coated with a white, furry covering with red projecting papillae (white strawberry tongue); by the third to fifth day, the white coat sloughs off, leaving a red swollen tongue (red strawberry tongue). 6. Tonsils are reddened, edematous, and covered with exudates. 7. Pharynx is edematous and beefy red. C. Interventions 1. Institute respiratory precautions until 24 hours after initiation of antibiotic therapy. 2. Provide ive therapy. 3. Provide bed rest. 4. Encourage fluid intake

ERYTHEMA INFECTIOSUM (FIFTH DISEASE) A. Description 1. Agent: Human parvovirus B19 2. Incubation period: 4 to 14 days; may be 20 days 3. Communicable period: Uncertain, but before the onset of symptoms in most children 4. Source: Infected person 5. Transmission: Unknown; possibly respiratory secretions and blood B. Assessment 1. before rash: Asymptomatic or mild fever, malaise, headache, runny nose 2. Stages of rash a. Erythema of the face (slapped-cheek appearance) develops and disappears by 1 to 4 days. b. About 1 day after the rash appears on the face, maculopapular red spots appear, symmetrically distributed on the extremities; the rash progresses from proximal to distal surfaces and may last a week or more. c. The rash subsides, but may reappear if the skin becomes irritated by the sun, heat, cold, exercise, or friction.

Interventions 1. Child is not usually hospitalized. 2. Pregnant women should avoid the infected individual. 3. Provide ive care. ister antipyretics, analgesics, and anti-inflammatory medications as prescribed.

INFECTIOUS MONONUCLEOSIS A. Description 1. Agent: Epstein-Barr virus 2. Incubation period: 4 to 6 weeks 3. Communicable period: Unknown 4. Source: Oral secretions 5. Transmission: Direct intimate B. Assessment 1. Fever, malaise, headache, fatigue, nausea, abdominal pain, sore throat, enlarged red tonsils 2. Lymphadenopathy and hepatosplenomegaly 3. Discrete macular rash most prominent over the trunk may occur. C. Interventions 1. Provide ive care. 2. Monitor for signs of splenic rupture H1N1 INFLUENZA A. Description 1. H1N1 is also known as swine flu and is a strain of influenza. 2. It is a viral infection that affects the respiratory system and is highly contagious. 3. Children, pregnant women, persons with preexisting health conditions, and persons with a compromised immune system are at high risk for developing complications.

4. It is caused by with an infected person or by touching something such as a toy or tissue that the infected person has touched. B. Prevention 1. H1N1 flu vaccine a. Children age 6 months and older need to be vaccinated. b. Children younger than 6 months are not old enough to receive the vaccine; family and caregivers need to get vaccinated. c. Children 9 years and younger need two doses at least 3 weeks apart; children 10 years and older need one dose (it takes about 2 weeks after receiving the second dose or the first dose in children needing only one dose before immunity develops). d. The H1N1 vaccine and seasonal flu vaccine can be given at the same time. e. A nasal spray version of the H1N1 vaccine that contains a weakened live virus may be given to people 2 to 49 years old who do not have a chronic health condition. 2. Wash the child’s hands frequently and teach handwashing techniques. 3. Avoid children who are ill. 4. Keep the child home from school or away from others until the child has been fever-free (without the use of antipyretics) for at least 24 hours.

IMMUNIZATIONS PRIORITY NURSING ACTIONS! Actions to Take When istering a Parenteral Vaccine 1. the prescription for the vaccine. 2. Obtain an immunization history from the parents and assess for allergies. 3. Provide information to the parents about the vaccine. 4. Obtain parental consent. 5. Check the lot number and expiration date and prepare the injection. 6. Select the appropriate site for istration. 7. ister the vaccine. 8. Document the istration and site of istration and lot number and expiration date of the vaccine. 9. Provide a vaccination record to the parents. The nurse should first the prescription and then obtain an immunization history from the parents to ensure that the immunizations are up to date. The nurse should also question the

parents about the presence of any allergies in the child because some vaccines contain components to which the child may be allergic. The nurse next provides information to the parents about the vaccine and obtains consent. The expiration date and the lot number (located on the medication vial) of the vaccine should be checked before preparing the vaccine for istration. When the vaccine is prepared, the nurse prepares the child for the procedure, selects an appropriate site, and isters the vaccine. The nurse documents that the vaccination has been istered and provides an updated immunization record to the parents. If there is suspicion that the parent will not bring the child to the pediatrician or health care clinic for follow-up immunizations according to the optimal immunization schedule, any of the recommended vaccines can be istered simultaneously. General contraindications and precautions 1. A vaccine is contraindicated if the child experienced an anaphylactic reaction to a previously istered vaccine or a component in the vaccine. 2. Live virus vaccines generally are not istered to individuals with severely deficient immune systems, individuals with a severe sensitivity to gelatin, or pregnant women. 3. A vaccine is istered with caution to an individual with a moderate or severe acute illness, with or without fever. RECOMMENDED CHILDHOOD AND ADOLESCENT IMMUNIZATIONS A. Hepatitis B vaccine (HepB) 1. Protects against hepatitis B 2. istered by the intramuscular route 3. First dose of hepatitis B vaccine (monovalent) should be istered soon after birth and before hospital discharge (the birth dose can be delayed in rare circumstances if the infant’s mother tests negative for hepatitis B surface antigen [HBsAg]). 4. Monovalent HepB or a combination vaccine containing hepatitis B may be used to complete the series. 5. The second dose is istered at age 1 to 2 months. 6. The final dose should be given at 24 weeks or older (6 to 18 months of age). 7. Contraindications: Severe allergic reaction to previous dose or vaccine component (components include aluminum hydroxide, yeast protein) 8. Precautions: An infant weighing less than 2000 g or an infant with moderate or severe acute illness with or without fever. 9. HBsAg-positive mothers a. Infant should receive HepB vaccine and hepatitis B immunoglobulin (HBIG) within 12 hours of birth. b. Infant should be tested for HBsAg and antibody to HBsAg after completion of HepB series (9 to 18 months of age).

B. Two vaccines are available (RotaTeq and Rotarix) 1. They are istered by the oral route because the vaccine must replicate in the infant’s gut. 2. Vaccine may be withheld if an infant is experiencing severe vomiting and diarrhea; it is istered as soon as the infant recovers. 3. RotaTeq: Three doses are needed; the first dose of the vaccine needs to be istered at age 6 to 14 weeks, the second is given 4 to 10 weeks after the first dose, and the third is given 4 to 10 weeks after the second dose (no later than 32 weeks of age). 4. Rotarix: Two doses are needed; the first dose of the vaccine needs to be istered at age 6 to 14 weeks, and the second is given 4 weeks after the first dose (series needs to be completed by 24 weeks of age). C. Diphtheria, tetanus, acellular pertussis (DTaP); tetanus toxoid; reduced diphtheria toxoid and acellular pertussis vaccine (Tdap adolescent preparation) 1. Protect against diphtheria, tetanus, and pertussis 2. istered by intramuscular route 3. DTaP is istered at 2, 4, and 6 months; between 15 and 18 months; and between 4 and 6 years of age. 4. The fourth dose of DTaP can be given at 12 months of age if 6 months have elapsed since the third dose and the child might not return for follow-up at 12 to 18 months of age. 5. The fifth (final) dose is istered at age 4 years or older. 6. The Tdap (adolescent preparation) is recommended at 11 to 12 years of age for children who have completed the recommended childhood DTaP series but have not received a tetanus and diphtheria toxoid (Td) booster dose; children 13 to 18 years old who have not received Tdap should receive a dose. 7. Td does not provide protection against pertussis; Td is used as a booster every 10 years after Tdap is istered at 11 to 18 years of age. 8. Encephalopathy is a complication. 9. Contraindications: Encephalopathy within 7 days of a previous dose or a severe allergic reaction to a previous dose or to a vaccine component. D. Haemophilus influenzae type b conjugate vaccine (Hib) 1. Protects against numerous serious infections caused by H. influenzae type b, such as bacterial meningitis, epiglottitis, bacterial pneumonia, septic arthritis, and sepsis 2. istered by intramuscular route 3. Hib is istered at 2, 4, and 6 months of age and between 12 and 15 months of age. 4. Depending on the brand of Hib vaccine used for the first and second doses, a dose at 6 months of age (third dose) may not be needed. 5. DTaP-Hib combination products should not be used for primary immunization in infants at 2, 4, or 6 months of age, but can be used as the final dose in children 12 months to 4 years of age. 6. Contraindications: Severe allergic reaction to a previous dose or vaccine component E. Influenza vaccine 1. Vaccine is recommended annually for children 6 months to 18 years of age. 2. Refer to Section XIV for information on the H1N1 influenza virus and the H1N1 vaccine.

F. Inactivated poliovirus vaccine (IPV) 1. IPV protects against polio. 2. IPV is istered by the subcutaneous route (may also be given by the intramuscular route) 3. IPV is istered at 2, 4, and 6 to 18 months and 4 to 6 years of age. 4. The last dose of the IPV should be istered on or after age 4 years and at least 6 months after the previous dose; additionally, if four doses are istered before age 4 years, a fifth dose should be istered at age 4 to 6 years. 5. Contraindications: Severe allergic reaction to a previous dose or vaccine component; components may include formalin, neomycin, streptomycin, or polymyxin B G. Measles, mumps, rubella (MMR) vaccine 1. MMR protects against measles, mumps, and rubella. 2. Vaccine is istered by the subcutaneous route. 3. The first dose of MMR is istered between 12 and 15 months of age; the second dose is recommended at 4 to 6 years of age (the second dose may be istered during any visit as long as at least 4 weeks have elapsed since the first dose). 4. Children who have not received the second dose previously should complete the schedule at the 11- to 12-year-old pediatric or health care clinic visit. 5. Contraindications: Severe allergic reaction to a previous dose or vaccine component (gelatin, neomycin, eggs), pregnancy, known immunodeficiency 6. If the child received immunoglobulin, the MMR vaccine should be postponed for at least 3 to 6 months (immunoglobulin can inhibit the immune response to the MMR vaccine). H. Varicella vaccine 1. Varicella vaccine protects against chickenpox. 2. It is istered by the subcutaneous route. 3. Varicella vaccine is istered at 12 and 15 months of age and again at 4 to 6 years of age. 4. Children 13 years old and older (who have not had chickenpox or have not been previously vaccinated) need two doses given at least 28 days apart. 5. Children receiving the vaccine should avoid aspirin or aspirin-containing products because of the risk of Reye’s syndrome. 6. Contraindications: Severe allergic reaction to a previous dose or vaccine component (gelatin, bovine albumin, neomycin), significant suppression of cellular immunity, pregnancy I. Pneumococcal conjugate vaccine (PCV) 1. PCV prevents infection with Streptococcus pneumoniae, which may cause meningitis, pneumonia,septicemia, sinusitis, and otitis media. 2. It is istered by the intramuscular route. 3. Vaccine can be given concurrently with other childhood vaccines at 2, 4, 6, and 12 to 15 months of age (the final dose in the series is given at age 12 months or older). 4. Pneumococcal polysaccharide vaccine (PPSV) is recommended in addition to PCV for certain high-risk groups, such as children with chronic illness specifically associated with

increased risk of pneumococcal disease or its complications; anatomical or functional asplenia; hemoglobinopathies; nephrotic syndrome; cerebrospinal fluid leaks; a cochlear implant; and conditions associated with immunosuppression (PPSV is given at least 8 weeks after the last dose of PCV). 5. Contraindications: Severe allergic reaction to a previous dose or vaccine component J. Hepatitis A vaccine (HepA) 1. Vaccine protects against hepatitis A. 2. Vaccine is recommended for all children at age 1 year (12 to 23 months); two doses should be istered at least 6 months apart (vaccination of children older than 23 months is allowed for those at increased risk). 3. It is istered by the intramuscular route. 4. Contraindications: Severe allergic reaction to a previous dose or vaccine component K. Meningococcal vaccine (MCV) 1. Vaccine protects against Neisseria meningitidis. 2. Meningococcal (MCV4) vaccine is the preferred type of vaccine and is given intramuscularly. 3. MCV4 should be istered to all children at age 11 to 12 years and to unvaccinated adolescents at high school entry (age 15 years); all college freshman living in dormitories should be vaccinated. 4. Revaccination is recommended for children who remain at increased risk after 3 years (if the first dose was istered at age 2 to 6 years) or after 5 years (if the first dose was istered at age 7 years or older). 5. It is contraindicated in children with a history of Guillain-Barre´ syndrome. L. Human papillomavirus vaccine (HPV) 1. Depending on the type of vaccine used (HPV2 or HPV4), the HPV vaccine guards against diseases that are caused by HPV types 6, 11, 16, and 18, such as cervical cancer, cervical abnormalities that can lead to cervical cancer, and genital warts. 2. The vaccine is most effective for boys and girls if istered before exposure to HPV through sexual . 3. The vaccine is istered as three injections over 6 months—first dose to girls at age 11 to 12 years, second dose 2 months after the first dose, and third dose 6 months after the first dose. 4. A three-dose series may be istered to boys 9 to 18 years old to reduce their likelihood of acquiring genital warts. 5. The vaccine can cause pain, swelling, itching, and redness at the injection site; fever; nausea; and dizziness. 6. The vaccine is contraindicated in individuals with a reaction to a previous injection and in pregnant women. Guidelines for istration of Vaccines 1. Follow manufacturer’s recommendations for route of istration, storage, and reconstitution of the vaccine.

2. If refrigeration is necessary, store on a center shelf and not on the door; frequent temperature changes from opening the refrigerator door can alter the vaccine’s potency. 3. A vaccine information statement needs to be given to the parents or individual, and informed consent for istration needs to be obtained. 4. Check the expiration date on the vaccine bottle. Parenteral vaccines are given in separate syringes in different injection sites. 5. Vaccines istered intramuscularly are given in the vastus ateralis muscle (best site) or ventrogluteal muscle (the deltoid can be used for children 36 months and older); the dorsogluteal site (buttocks) is avoided. 6. Vaccines istered subcutaneously are given into the fatty areas in the lateral upper arms and anterior thighs. 7. Adequate needle length and gauge are as follows: intramuscular, inch, 23-25 gauge; subcutaneous, ⅝ inch, 5 gauge (needle length may vary depending on the child’s size). 8. Mild side effects include fever, soreness, swelling, or redness at injection site. A topical anesthetic may be applied to injection site before the injection. 9. For painful or red injection sites, advise the parent to apply cool compresses for the first 24 hours, and then use warm or cold compresses as long as needed. 10. An age-appropriate dose of acetaminophen (Tylenol) or ibuprofen (Motrin) may be istered every 4 to 6 hours for vaccine-associated discomfort. 11. Maintain an immunization record—document day, month, year of istration; manufacturer and lot number of vaccine; name, address, title of person istering the vaccine; and site and route of istration. 12. A vaccine adverse event report needs to be filed and the health department needs to be notified if an adverse reaction to an immunization occurs.

REACTIONS TO A VACCINE A. Local reactions 1. Tenderness, erythema, swelling at injection site 2. Low-grade fever 3. Behavioral changes such as drowsiness, unusual crying, decreased appetite B. Minimizing local reactions 1. Select a needle of adequate length to deposit vaccine deep into the muscle or subcutaneous mass. 2. Inject into the appropriate recommended site Anaphylactic reactions 1. Goals of treatment are to secure and protect the airway, restore adequate circulation, and prevent further exposure to the antigen. 2. for a mild reaction with no evidence of respiratory distress or cardiovascular compromise, a subcutaneous injection of an antihistamine, such as diphenhydramine (Benadryl), and epinephrine (Adrenalin) may be istered. 3. Formoderate or severe distress, establish an airway; provide cardiopulmonary resuscitation if the child is not breathing; elevate the head; ister epinephrine, fluids, and vasopressors as prescribed; monitor vital signs; and monitor urine output.

Refrences:-

1. K Park ‘’ Textbook Of Preventive And Social Medicine’’ ,20th Edition , 2009 , BanarsidasBhanot Publication , Page No: 232-258 2. Bagga and Paul. Ghai essential pediatrics. .Eighth edition. 2013, CBS publishers and distributors pvt. Limited. Page no-235-270 3. Mahajan & Gupta. Textbook of Preventive and Social Medicine 4th edition, 2013, jaypee publication, 179-204 4. Linda Anne Silvestri. Saunders comprehensive review for the nclex-rn examination, 5th Edition 2011, Elsevier Publication, 250,548-560 Net:      

http://www.intelihealth.com/IH/ihtIH/EMIHC000/20722/8632/187947. http://www.chadd.org. www.unicef.org/india/health_369.html

http://en.wikipedia.org/w/index.php http://www.slideshare.net/LiniVivek/imnci-intregrated-management-of-neonataland-childhood-iliness http://www.slideshare.net/drprabhakar/imnci-29188754?related=1