This document provides information on common infectious diseases including malaria, dengue fever, measles, mumps, and tuberculosis. It discusses the causative agents, signs and symptoms, transmission, diagnosis, and treatment of these diseases. Malaria remains a major public health issue in developing countries, causing over 1 million deaths annually. Measles is highly contagious and a leading cause of death in children under 5 despite available vaccines. Mumps is transmitted through saliva and commonly causes swelling of the salivary glands.

1. COMMUNICABLE DISEASES
Aparna,
Clinical Instructor
FNCON, GTBH

2. Common Infectious Diseases
COMMON FEVERS
• Malaria
• Dengue fever
• Typhoid fever
EXANTHEMATOUS FEVERS
• Measles
• Mumps
• Chickenpox
• Rubella
CHRONIC INFECTIONS
• Tuberculosis
• HIV

3. MALARIA
• Malaria is an acute and chronic illness characterized by paroxysms of
fever, chills, sweats, fatigue, anemia, and splenomegaly.
• Malaria is of overwhelming importance in the developing world
today, with an estimated 300 to 500 million cases and more than 1
million deaths each year.
• Most malarial deaths occur among infants and young children.
• Season: most common in July-November
• Definitive host: Anopheles mosquito
• Intermediate host: Man Vector:
Anopheles culicfacies(rural)
Anopheles stephensi (urban)

4. INCUBATION PERIOD
TYPE INCUBATION PERIOD
P vivax 8-17 days (14days)
P Falciparum 9-14 days (12 days)
P Malariae 18-40 days (28 days)
P Ovale 16-18days (17DAYS)

5. PHASES

7. SYMPTOMS
• Impaired consciousness Prostration
• Multiple seizures Respiratory distress
• Pulmonary edema Jaundice
• Hemoglobinuria Abnormal bleeding
• Severe anemia Circulatory collapse
• The most common serious complication is severe anemia.
• Serious complications that appear unique to P. falciparum include
cerebral malaria, acute renal failure, respiratory distress from
metabolic acidosis, algid malaria and bleeding diatheses.
• P. falciparum is the most severe form of malaria and is associated
with higher density parasitemia and a number of complications

8. CLINICAL MANIFESTATIONS

9. DIAGNOSIS
• The diagnosis of malaria Giemsa-stained smears of peripheral blood
or rapid immunochromatographic assay.
• Stains used for diagnosis Giemsa stain >Wright stain or Leishman
stain. Thick and Thin blood smears
• The concentration of erythrocytes on a thick smear is 20-40 times
that on a thin smear and is used to quickly scan large numbers of
erythrocytes.
• The thin smear allows for positive identification of the malaria
species and determination of the percentage of infected erythrocytes
and is useful in following the response to therapy.
• Most symptomatic patients with malaria will have detectable
parasites on thick blood smears within 48 hr.

10. MANAGEMENT
New Treatment plan is clinically divided into two
1. Uncomplicated malaria
• Chloroquine for 3 days (Day 1: 10 mg/kg + Day 2: 10 mg/kg + Day 3:
5mg/kg) + Primaquine 0.25 mg/kg daily for 14 days
• Uncomplicated P. falciparum- Artesunate (4 mg/kg body weight) daily
for 3 days and sulfadoxine pyrimethamine (25 mg/kg + 1.25 mg/kg
body weight) on Day 0; + Primaquine 0.75 mg/kg body weight single
dose on day 2
• Mixed Infections (P. vivax + P. falciparum)- Full course of artemisinin-
based combination therapy (ACT) + Primaquine 0.25 mg/kg daily for
14 days India

11. Complicated malaria
Initial treatment
• Parenteral Artemisin derivatives (Artesunate, Artemether, Arteether)
or Parenteral Quinine Once patient can take Oral therapy
• Those on parenteral Artemisin derivatives: oral ACT(full course) ACT-
Artesunate Sulfalene Pyrimethamine Combination Therapy
• Those on parenteral Quinine: oral quinine+Doxycycline 7 days
Complicated malaria in pregnancy I trimester: parenteral quinine II
and III trimester: Parenteral Artemisin derivatives

12. PREVENTION
National Vector Borne Disease Control Program
• Early case detection and prompt treatment (EDPT):
• Vector control:
• Mosquitoes in the community can be controlled with the
combination of multiple activities such as chemical and biological
control.
• Personal protective measures against mosquito bites:
• Use of mosquito repellent creams, liquids, coils, mats etc.
• Screening of the houses with wire mesh
• Use of bed nets pretreated with insecticide
• Wearing clothes that cover maximum surface area of the body
• Environment management and community awareness about detection
of mosquito breeding places and their elimination.

13. DENGUE FEVER
• Dengue is the most rapidly spreading mosquito-borne viral disease in
the world
• Increase in incidence by over 30-fold in the last 50 years
• Currently endemic in all continents except Europe
ETIOLOGY THE VIRUS
• DEN- family flaviviridae genus flavivirus
• Has four distinct serotypes (DEN1 – 4)
• DEN-2 and DEN-3 cause severe disease
• Cleaved by host and viral proteases into 3 structural proteins and 7
nonstructural proteins(NS)

14. THE VECTOR
• Transmitted by infected Aedes mosquitoes
• Highly urbanized, fresh water, day feeding mosquito
THE HOST
• Humans are the primary host of the virus
• Severity depends upon factors like gender,secondary infection,age
and chronic diseases (sickle cell anemia, asthma , DM)
• Vertical transmission and through infected blood products

17. PATHOGENESIS
Capillary damage
Fluid leaks into extravascular spaces
Hemoconcentration, Hypovolemia
Increased cardiac work
Tissue hypoxia,metabolic acidosis
THROMBOCYTOPENIA
+
LIVER DAMAGE
+
DIC
DENGUE HAEMORRHAGIC FEVER

18. CLINICAL MANIFESTATIONS

19. DIAGNOSIS
• ELISA- based antigen detection test (NSI) from first day onwards.
• Antibody detection test, IgM capture ELISA for diagnosing the cases
after the fifth day of onset of disease.

24. MEASLES (Rubeola)
It remains a leading cause of death among young children globally,
despite the availability of a safe and effective vaccine. An estimated
197,000 people died from measles in 2007, mostly children under the
age of five .
• It is an acute viral infection characterized by a maculopapular rash
erupting successively over the neck, face, body, and extremities and
accompanied by a high fever.

25. Causative Agent
•Paramyxoviridae family
• There is only one serotype of
Measles virus and no subtypes
have yet been recognized

26. EPIDEMIOLOGY
Infection sources
• Patients of acute stage and viral carriers of atypical measles
Transmission
• Highly contagious, approximately 90% of susceptible contacts acquire
the disease.
• Respiratory secretions: maximal dissemination of virus occurs by
droplet spray during the prodromal period (catarrhal stage).
• Contagious from 5 days before symptoms, 5 days after onset of rash
• Seasons: in the spring, peak in Feb-May

27. PATHOGENESIS
Portal of entry
• Respiratory tract and regional lymph nodes
• Enters bloodstream (primary viraemia) monocyte – phagocyte
system target organs (secondary viraemia)
Target organs
• The skin; the mucous membranes of the nasopharynx, bronchi, and
intestinal tract; and in the conjunctivae, ect

28. RESULTS IN..
• Koplik spots and skin rash: serous exudation and proliferation of
endothelial cells around the capillaries
• Conjunctivis
• Laryngitis, croup, bronchitis :general inflammatory reaction
• Hyperplasia of lymphoid tissue: multinucleated giant cells (Warthin-
Finkeldey giant cells) may be found
• Interstitial pneumonitis: Hecht giant cell pneumonia.
• Bronchopneumonia: due to secondary bacterial infections
• Encephalomyelitis: perivascular demyelinization occurs in areas of
the brain and spinal cord.
• Subacute sclerosing panencephalitis(SSPE): degeneration of the
cortex and white matter with intranuclear and intracytoplasmic
inclusion bodies

30. CLINICAL MANIFESTATION
Typical Manifestation:
Patients havn’t had measles immunization, or vaccine failure with
normal immunity or those havn’t used immune globulin
Incubation period (infection to symptoms) :
• 6-18days (average 10 days)
Prodromal period:
• 3-4 days
• Non-specific symptoms: fever, malaise, anorexia, headache
• Classical triad: cough, coryza, conjunctivitis (with photophobia,
lacrimation)

31. Koplik’s spot
• 24-48 hr before rash appears
• 1mm, grayish white dots with slight,
reddish areolae
• Buccal mucosa, opposite the
lower 2nd molars
• Increase within 1day and spread
• Fade soon after rash onset
Rash
• 3-4days
• Erythematous, non-pruritic,
maculopapular
face trunk arms and legs feet

32. • Temperature:
• Rises abruptly as the rash appears
• Reaches 40℃ or higher
• Settles after 4-5 days – if persists, suspect secondary infection
• Coryza, fever, and cough: Increasingly severe up to the time the rash
has covered the body
• Lymphadenopathy (posterior cervical region, mesenteric)
splenomegaly, diarrhoea, vomiting

33. COMPLICATIONS
Respiratory Tract
• Laryngitis, tracheitis, bronchitis – due to measles itself
• Laryngotrachobronchitis (croup) –cause airway obstruction to require
tracheostomy
• Secondary pneumonia – immunocompromised, malnourished
patients. pneumococcus, group A Streptococcus, Staphylococcus
aureus and Haemophilus influenzae type B.
• Exacerbation of TB
Myocarditis
Malnutrition and Vitamin A deficiency

34. CNS
• The incidence of encephalomyelitis is 1-2/l,000 cases of measles
• Onset occurs 2-5 days after the appearance of the rash
• No correlation between the severity of the rash illness and that of
the neurologic involvement
• Earlier - direct viral effect in CNS
• Later – immune response causing demyelination
• Significant morbidity, permanent sequelae – mental retardation and
paralysis
• Subacute sclerosing panencephalitis (SSPE):
• extremely rare, 6-10 years after infection. Progressive dementia, fatal
Interaction of host with defective form of virus

35. DIAGNOSIS
• Isolation of measles virus from a clinical specimen (e.g. nasopharynx,
urine)
• Significant rise in measles IgG by any standard serologic assay
• Positive serologic test for measles IgM antibody
• Immunofluorescence detects Measles antigens
• Multinucleated giant cells in smears of nasal mucosa
• Low white blood cell count and a relative lymphocytosis in PB
• Measles encephalitis – raised protein, lymphocytes in CSF

36. DIFFERENTIAL DAGNOSIS
The rash of measles must be differentiated from that of
• rubella;
• roseola intantum;
• enteroviral infections;
• scarlet fever;
• and drug rashes.
SCARLET FEVER

37. TREATMENT
• Supportive, symptom-directed
• Antipyretics for fever
• Bed rest
• Adequate fluid intake
• Be protected from exposure to strong light
• Antibiotics for otitis media, pneumonia
• High doses Vitamin A in severe/ potentially severe measles/ patients
less than 2 years: 100,000IU—200,000IU

38. PREVENTION
Quarantine period
• 5 days after rash appears, longer for complicated measles
Vaccine
• The initial measles immunization (MR-1)is recommended at 9-12mo
of age
• A second dose of immunization (MR-2) is recommended at 16-
24months of age because about 15% of vaccinated children fail to
develop immunity from the first dose.
Postexposure Prophylaxis
• Passive immunization with immune globulin (0.25mL/kg) is effective
for prevention and attenuation of measles within 5 days of exposure.

39. Nursing Diagnosis
• Acute Pain may be related to inflammation of mucous membranes,
conjunctiva, and presence of extensive skin rash with pruritus,
possibly evidenced by verbal reports, distraction behaviors, self-
focusing, and autonomic responses (changes in vital signs).
• Hyperthermia may be related to presence of viral toxins and
inflammatory response, possibly evidenced by increased body
temperature, flushed/warm skin, and tachycardia.
• Risk for [secondary] Infection: risk factors may include altered
immune response and traumatized dermal tissues.*
• Deficient Knowledge regarding condition, transmission, and possible
complications may be related to lack of information/
misinterpretation, possibly evidenced by statements of concern,
questions, misconceptions, and development of preventable
complications.

40. MUMPS
• Mumps is a vaccine-preventable disease. 121 countries or 62%
countries of the world have included mumps vaccine in their routine
schedule in the form of MMR vaccine.
• Seasonal disease of winter and spring.
• Mainly affects salivary glands and also known as infective parotitis.
Commonly seen in children from 5-9 yrs and young adults
• Caused by virus of paramyxoviridae family.
• Virus has been isolated from saliva as long as 6 days before and up to
9 days after appearance of salivary gland swelling.
• Transmission occurs within 24 hr before the appearance of the
swelling or later within 3 days after it has subsided. Virus has been
isolated from urine from the 1st- 14th day after the onset of salivary
gland swelling.

41. Pathogenesis
After entry into the last and initial multiplication in the cells of the
respiratory tract, the virus is bloodborne to many tissues, among which
the salivary and other glands are the most susceptible
The incubation period ranges from 14-24 days, with a peak at 17-18
days.
Approximately 30-40% of infections are subclinical.

42. Clinical manifestations
• Prodromal manifestations are Fever, Muscular pain (especially in the
neck), Headache, Malaise typically precede the parotid swelling by 12
to 24 hours.
• Common signs are Earache on the side of parotid involvement,
Discomfort with eating or drinking acidic food, Parotid pain
• Edematous and erythematous buccal mucosa,Trismus (spasm of the
masticatory muscles) can occur.
• Presternal edema, Morbilliform rash.
• Systemic symptoms include fever, usually resolve within 3 to 5 days,
the parotid swelling subsides within 7 to 10 days.
• Adolescents and adults have more severe disease than young
children

44. DIAGNOSIS
• Complete blood cell count (CBC) – A complete blood cell count
reveals a normal, decreased, or elevated white blood cell (WBC)
count, with predominating lymphocytes in differential count.
• Inflammatory markers-Sera inflammatory markers, such as C-reactive
protein or erythrocyte sedimentation rate (ESR), can be elevated to
show a nonspecific systemic inflammatory response.
• Serum amylase is elevated in mumps parotitis (amylase-S) and in
pancreatitis (amylase-P). Serum lipase is elevated in pancreatitis.
• Specific immunoglobulin-positive mumps-specific immunoglobulin M
(IgM) titer or rise in mumps-specific immunoglobulin G (IgG)
antibody titers between acute and convalescent sera specimens.
• For diagnosis, an assay for the detection of mumps-specific
immunoglobulin M antibodies in serum and oral fluid specimens is
commercially available.

45. • Mumps virus can be isolated from nasopharyngeal swabs, blood, and
fluid from the buccal cavity typically within the period of seven days
before and nine days after, the onset of parotitis.
• Lumbar puncture- If meningitis or encephalitis is suspected, a lumbar
puncture to obtain CSF (cerebrospinal fluid) for examination may be
considered to clarify cause.
• Auditory testing is indicated to assess for development of a hearing
impairment.
• Scrotal ultrasonography must be performed when orchitis is clinically
suspected to rule out testicular torsion.

46. MANAGEMENT
• Conservative, supportive medical care is indicated. mumps is a self-limited
disease.
• Analgesics (acetaminophen, ibuprofen) may be used for headaches or
discomfort due to parotitis.
• Topical application of warm or cold packs to the swollen parotid area may
be used to soothe the painful area.
• A light diet with plenty fluid intake is encouraged.
• Acidic foods (such as tomato, vinegar-containing food additives) and liquids
(such as orange juice) should be avoided to lessen oral pain and discomfort.
• Stronger analgesics may be required for patients with orchitis with bed rest,
scrotal support, and ice packs. Mumps without associated major
complications can be managed on an outpatient basis.
• It is advised to follow good hand washing practices.
• Isolation for 5 days from the onset of symptoms.

47. COMPLICATIONS
• Meningitis: Aseptic meningitis occurs in 10% of patients with mumps.
• Encephalitis: Encephalitis occurs rarely (0.02–0.3% of cases). Case–
fatality rate of mumps encephalitis is low, permanent sequelae,
including paralysis, seizures, cranial nerve palsies, aqueductal
stenosis and hydrocephalus, may occur.
• Orchitis: Inflammation of one or both testicles occurs in 20% of
postpubertal males who develops mumps.
• Oophoritis: Females who have reached puberty may have
inflammation in the ovaries (oophoritis) or breasts (mastitis).
• Hearing loss: Cranial nerve involvement (especially eighth cranial
nerve damage) is one of the leading causes of deafness in childhood,
affecting approximately 5/100000 mumps patients.
• Pancreatitis is reported as a complication in approximately 4% of
cases.

48. PREVENTION
VACCINATION
IAP recommends MMR at 9 months of age (measles containing vaccine
ideally should not be administered before completing 270 days or 9
months of age), second dose at 15-18 months and third dose at 4-6
years of age.
Contraindication
• Individuals with advanced immune deficiency.
• Mumps vaccination is contraindicated during pregnancy.
• Allergy to vaccine components, such as neomycin and gelatin, is a
contraindication to administration of the vaccine.

49. Prevention of transmission
• Patients diagnosed with mumps should stay away with others for at
least 5 days from the onset of symptoms.
• Encourage the patient for good hand washing practices.
• Encourage the patient to cover mouth and nose during coughing and
sneezing with tissue, (put used tissue in the trash can) and if tissue is
not available cover with upper sleeve or elbow, not the hands.
• Drinks and eating utensils of patient should not be shared by others.
• Frequently touched surfaces, such as toys, doorknobs, tables,
counters should be kept clean.

50. RUBELLA
• Human specific RNA virus
• Family : togavirus
• Rate of fetal infection by maternal infection is high in first 12
weeks
Transmission:
• Vertical transmission: maternofetal

52. Rubella Clinical Manifestation
• It is characterized by constellation of Cataract, SNHL and Congenital
heart disease
• Common cardiac defects: patent ductus arteriosus and pulmonary
artery stenosis
• Early features: IUGR, retinopathy, microphthalmia,
meningoencephalitis, electroencephalographic abnormalities,
hypotonia, dermatoglyphic abnormalities,thrombocytopenic purpura
and diabetes mellitus
• Rare Complications: myocarditis, glaucoma, microcephaly, chronic
progressive panencephalitis, hepatitis, anemia, thyroid abnormality,
cryporchidism, polycystic kidney

53. Rubella Infection

54. Rubella Diagnosis
Antenatal Diagnosis: in neonates
• Severe fetal abnormality occurs in first 16 weeks of gestation if
maternal rubella infection is acute
• Determination of specific IgM in fetal blood
• Direct inoculation of rubella antigen and RNA in a chorionic villus
biopsy specimen
Postnatal Diagnosis: in neonates
• Isolation of rubella virus (oropharynx, urine)
• Detection of rubella specific IgM in cord or neonatal blood
• Persistent rubella specific titers over time

55. Rubella Treatment and Prevention
• Termination of pregnancy advised if infection occurs during the
first 5 months of pregnancy
• After birth symptomatic treatment to neonate
• Immunization to Rubella vaccine in susceptible woman
• Avoid conception for 3 months after receiving immunization
• Avoid breast feeding in mothers receiving Rubella vaccine

56. CHICKENPOX
• Chicken pox is a viral skin infection caused by varicella-zoster virus.
Most people regard chickenpox as a mild disease, but It is highly
contagious and present with rapid onset fever, centripetal rash and
constitutional symptoms.
• Chickenpox may appear after 10 to 21 days of contracting the viral
infection and usually lasts for ten days.
• Child is infective from 2 days before appearance of rash

59. COMPLICATIONS
• Secondary bacterial infection of the skin and mucosal membrane
• Neurological illness e.g. Paralysis or abdominal movements
• Pneumonia
• Reye’s syndrome
TREATMENT
• Largely symptomatic and supportive
• Hygiene must be optimised
• Sedatives and anti pruritic agents for itching.
• Paracetamol for fever
• Acyclovir given only to adolescents: 20mg/kg (max800mg/dose) QID for
5 days.

60. PREVENTION
• ISOLATION: until the day vesicles have crusted, religious
handwashing.
• CARE OF EXPOSED PERSON: chickenpox vaccine within 48hrs of
exposure may prevent varicella. VZIG immunoglobulins may prevent
illness if given within 7days of contact.
• ACTIVE IMMUNIZATION: live vaccine is available. 2 doses 4-8weeks
apart in adolescents and adults.

61. HERPES SIMPLEX VIRUS
• A life long infection, double stranded DNA
• Types: HSV-1 and HSV-2
• Source: secretion of skin, eye, mouth of infected person , contagious
spread
Transmission
• Intrapartum transmission: high risk with ruptured membrane (>4
hours), use of direct method for fetal monitoring and while passing
through birth canal
• Antenatal transmission: In utero infection either by transplacental or
ascending route
• Postnatal transmission: contact with oropharyngeal shedding of
infected person or maternal breast lesions.

62. HSV Clinical Manifestations
Skin, eye, and mouth infection: Vesicles typically appears on 6th to 9th
day of neonatal life.
CNS infection:
• 1/3 rd of neonates present with encephalitis, lethargy, seizures,
temperature instability and hypotonia.
• 2/3 rd of surviving infants have impaired neurodevelopment
Disseminated infection: Pneumonitis and fulminant hepatitis.
• Symptoms include seizures, shock, respiratory distress, disseminated
intravascular coagulation, respiratory failure

63. Herpes Simplex

64. HSV Diagnosis
• Viral isolation or fluorescent antibody detection of viral protiens :
Swabs of mucocutaneous, oropharynx, nasopharynx, conjuctivae
or samples of stool, urine and CSF are evaluated for presence of
HSV.
• Laboratory abnormalities: elevated hepatic transaminase levels,
direct hyperbilirubinemia, neutropenia, thrombocytopenia and
coagulopathy.
• Electroencephalography and CT/MRI : to detect HSV encephalitis
• X- ray : A diffuse interstitial pattern shows HSV pneumonitis

65. HSV Treatment
• Neonate with skin, eye and mouth infection
• Acyclovir 20 mg/kg Q8hrly for 14 days
• Neonate with CNS and disseminated disease
• Continue Acyclovir for 21 days

66. Management of neonate born to HSV positive
mother
• Consider elective Caesarean section, regardless of lesion status at
delivery, or if membranes rupture less than 4hrs.
• Swab infant’s conjunctivae and nasopharynx, and possibly collect urine
for DFA and culture to determine exposure to HSV
• Treat with acyclovir if DFA or culture positive or signs of neonatal HSV

67. HSV Prevention
• Avoid intercourse with HSV-2 positive partner in the third
trimester.
• Caesarean section in case of active lesion.
• Contact isolation of neonate born to HSV infected mother.
• Maintain strict hand washing.
• Use of gloves and mask.
• Avoid breast feeding in case of breast lesion.

68. Tuberculosis
• Agent : Mycobacterium Tuberculosis
• Reservoir of Infection: Sputum, Nasopharyngeal Secretions, fomites
• Mode of Transmission: Droplet, Airborne Transmission and
Transplacental route
• Incubation Period: 4-8weeks

69. Clinical Manifestations
• Onset is insidious
• Primary focus: the point of entry of the tubercle bacilli.
• Moderate to high grade fever with evening rise.
• Lethargy, loss of interest in play.
• Productive cough
• Reduced weight and appetite.
• Pain on affected side of chest.
• Hepatic and splenic enlargement, respiartory distress, fever,
lymphadenopathy, abdominal distention, lethargy and irritability, ear
dicharge and skin papules

70. • Pleural Effusion: intercostal spaces appear full, trachea is
shifted to the other side.
• Miliary Tuberculosis: dyspnea, delirium, convulsions and
miliary mottling on chest
• Abdominal Tuberculosis: colicky abdominal Pain, vomiting,
constipation. Irregular nodular masses, frank ascites,
intestinal obstruction, hepatosplenomegaly.
• Tubercular Meningitis:
Stage1 : fever
Stage2: neck rigidity, altered LOC, convulsions
Stage 3: deep coma, abnormal central respiration

71. DIAGNOSIS
• Laboratory Test:
oStains for AFB and cultures performed on blood, urine, three early
morning gastric aspirates, tracheal aspirates and CSF
• Radiologic Test:
oChest X-Ray (to detect infiltrates or milliary pattern)
• Tuberculin Skin Test: Mantoux test recommended for
children less than 5 years

72. PRINCIPLES OF MANAGEMENT
• Early detection and management
• Prompt, adequate, vigorous and prolonged(if required) management.
• Nutrition of child should be improved. Supplement vitamins and
minerals.
• Prevent and treat vigorously intercurrent infections.
• Trace reservoir of infection.
• Improve sanitation, and hygiene measures.
PREVENTION
• Vaccination : BCG (0.1ml) intradermally at birth.
• Tracing source infection and health education.

73. MANAGEMENT: COMPONENTS OF DOTS
1. Good quality diagnosis, through sputum microscopy
2. Directly observed treatment
3. Uninterrupted supply of good quality drugs
4. Systematic monitoring and accountability
5. Political and administrative commitment

74. MANAGEMENT (DOTS)
Phases of management
• INTENSIVE PHASE:
2 months. Eliminate bacterial load and prevent emergence
of drug resistant strains. Initiate treatment with atleast 2
antibacterial drugs.
• CONTINUATION PHASE:
4-6 months. Treat with atleast 2 antibacterial drugs to
continue and complete the treatment.

75. MANAGEMENT
• Treatment: Under DOTS program
Drugs Dose (mg/kg/day) Frequency
Isoniazid 5 q24h
Rifampicin 10 q24h
Streptomycin 10-30 q24h
Ethambutol 15-25 q12h
Pyrazinamide 25-35 q24h

76. Tuberculosis :Clinical Category
Categories As per WHO Suggested Regimes
Category 1 New Sputum positive
Pulmonary TB
Serious Extrapulmonary
2HRZE+4HR
Or
2SHRZ+4HR
Category 2 Relapse
Treatment failure
Interrupted treatment
2SHRZE+1HRZE+5HRE
Category 3 Negative sputum
Extrapulmonary TB
2HRZ+4HR

77. References
• Ghai Essentials of Pediatrics, OP Ghai, Seventh Edition, 2009, page
no.181-221
• Wong’s Essentials of pediatric nursing, 2nd south Asia Edition,
2017, pg no: 819-26, 813.
• Lippincott Manual of Neonatal Care, Williams and Wilkins, 7 th
edition; 2012, page no: 589- 682.
• Essential pediatric nursing, Piyush Gupta, 4th edition, CBS
Publishers, pg:258-281.
• www.who.int/biologicals/vaccines/mumps/en/
• www.who.int/immunization/monitoring_surveillance/burden/vpd/su
rveillance_type/