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Infectious Disease

The document discusses infectious diseases in children, focusing on respiratory tract infections, which are categorized into upper and lower respiratory tract infections. It details common conditions such as tonsillopharyngitis, otitis media, croup, and bronchiolitis, including their epidemiology, clinical features, diagnosis, and treatment options. The document highlights the importance of recognizing and managing these infections due to their prevalence and potential complications in pediatric populations.

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0% found this document useful (0 votes)
5 views148 pages

Infectious Disease

The document discusses infectious diseases in children, focusing on respiratory tract infections, which are categorized into upper and lower respiratory tract infections. It details common conditions such as tonsillopharyngitis, otitis media, croup, and bronchiolitis, including their epidemiology, clinical features, diagnosis, and treatment options. The document highlights the importance of recognizing and managing these infections due to their prevalence and potential complications in pediatric populations.

Uploaded by

hermelawl12
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd

UNIT 2

Infectious disease in children

Respiratory tract infection


Introduction
Acute respiratory infections (ARIs)
are classified as upper respiratory
tract infections (URIs) and lower
respiratory tract infections (LRIs).
URIs consists of infections of
airways from the nostrils to larynx,
including the paranasal sinuses and
the middle ear.
LRTs represents infection below the
larynx from the trachea and bronchi
to the bronchioles and the alveoli.
Introduction
ARIs are the most common causes
morbidity and mortality in children
under five.
On average children under 5 have
three to six episodes of ARIs
annually regardless of their
economic situation.
URIs includes;
 Common cold
 Sinusitis
 Otitis media
 Tonsillopharyngitis,
 Epiglottitis,
 Infectious Croup
LRIs includes;
 Bronchiolitis
 Pneumonia
Tonsillopharyngitis
(pharyngitis )
Pharyngitis refers to inflammation of
the structures of the pharynx, the
tonsils (if present) are most often
affected
Etiology; The commonest is a viral.
The most important viral agents
includes adenoviruses, coronaviruses,
enteroviruses, rhinoviruses, and
respiratory syncytial virus
 Group A β-hemolytic streptococcus
(GABHS) are the most common
bacterial cause.
Epidemiology
Viral URTs are spread by close
contact and occur most
commonly in fall, winter, and
spring.
Streptococcal pharyngitis
Illness occurs most often in
winter and spring and spreads
among siblings and classmates.
Clinical features/Viral pharyngitis
The onset of viral pharyngitis
may be more gradual, and
symptoms more often include
rhinorrhea, cough, and diarrhea.
A viral etiology is suggested by
the presence of conjunctivitis,
coryza, hoarseness, and cough.
Viral pharyngitis is generally
mild.
GABHS pharyngitis
Streptococcal pharyngitis is
relatively uncommon before 2-3 yr of
age, has a peak incidence in the early
school years.
Infection occurs following Colonization
of the pharynx by the
microorganisms.
The M protein is the major virulence
factor of GABHS and facilitates
resistance to phagocytosis by
polymorphonuclear neutrophils.
GABHS pharyngitis/Clinical features
The incubation period is 2-5 days.
The onset of streptococcal pharyngitis is
often rapid with prominent sore throat
and fever in the absence of cough.
Headache and gastrointestinal symptoms
(abdominal pain, vomiting) are common.
The pharynx is red, and the tonsils are
enlarged and classically covered with a
yellow, blood-tinged exudate.
the uvula may be red, stippled, and
swollen.
The anterior cervical lymph nodes are
A culture positive case of
Streptococcal pharyngitis with typical tonsillar
exudate
Diagnosis
Throat culture remains an imperfect gold
standard for diagnosing streptococcal
pharyngitis.
 False-positive:
 If other organisms are misidentified as
GABHS
 streptococcal carriers can also have positive
cultures.
 False-negative;
 Inadequate throat swab specimens.
 patients’ use of antibiotics
• Rapid streptococcal antigen test -is highly
specific but less sensitive.
Treatment
• Most untreated episodes of
streptococcal pharyngitis resolve
uneventfully in a few days.
• Early antibiotic therapy hastens
clinical recovery by 12-24 hr.
The primary benefit of treatment is
the prevention of acute rheumatic
fever, if antibiotic is given within 9
days of illness.
GABHS remains universally
susceptible to penicillin.
Treatment continued…
Oral Augmentin/amoxicillin for 7_10
days, or
A single intramuscular dose of
benzathine penicillin (600,000U for
children <27 kg 1.2 million U for larger
children and adults).
For patients allergic to penicillin,
treatment options include Erythromycin,
Azithromycin and Clindamycin.
Specific therapy is unavailable for most
viral pharyngitis.
Otitis Media(OM
Otitis Media is defined as an
inflammation of the middle ear
Acute otitis Media(AOM) is an acute
infection of the middle ear.
It is the most common cause of
hearing loss in children.
The definition of AOM includes:
Recent, usually abrupt, onset of signs
and symptoms of middle-ear
inflammation(TM) and middle ear
effusion (MEE).
Epidemiology

Over 80% of children will have


experienced at least one episode
of otitis media (OM) by the age of
3 yr.
The peak incidence and
prevalence of OM is during the
1st 2 yr of life.
Incidence greater in boys than in
girls
Etiology
Three pathogens predominate in
AOM;
 Streptococcus pneumoniae(30-
50%)
 nontypeable Haemophilus
influenzae(40-50%)
 Moraxella catarrhalis(10%).
pathogenesis
• Infection mostly occurs in infants
and children because of the
shorter and more horizontal
orientation of the Eustachian
tube which allows reflux from the
pharynx.
Clinical manifestation
•In young children, evidence of ear
pain may be manifested by irritability
or a change in sleeping or eating
habits and occasionally, holding or
tugging at the ear .
Fever , Crying,
Rupture of the tympanic membrane
with purulent otorrhea is uncommon.
Symptoms associated with upper
respiratory tract infections also occur.
Hearing loss
Diagnosis
Isbased on the history and
otoscopic examination which
demonstrate red, inflamed
bulging or perforated ear drum.
Acute Otitis Media-TM
Complication of OM
Acute mastoiditis – infection of
the mastoid process.
Tympanic membrane perforation.
Hearling loss.
Meningitis.
Brain abscess.
Treatment
Individual episodes of AOM
should be treated with
antimicrobial drugs’
Amoxicillin for 10 days –first line
 Amoxicillin-clavulanate-second
line for 10days.
Quinolone for COM
Infectious Upper Airway
Obstruction
Croup
Epiglottitis
Introduction
Upper airway obstruction is a common
cause of pediatric emergency department
visits, accounting for approximately 15% of
all critically ill patients.
Infectious etiologies account for 90% of
these, with viral croup accounting for 80%.
Epiglottis accounts for 5% of severe cases.
Other significant causes include other
infections etiologies (bacterial tracheitis,
tonsillar pathology and diphtheria)
Croup Syndrome
Definition

The term croup refers mainly acute and


infectious processes that are characterized
by a bark-like cough and may be
associated with hoarseness, inspiratory
stridor, and respiratory distress.
Croup also called
laryngotracheobronchitis.
Croup typically affects the larynx, trachea,
and bronchi.
Most common cause of infectious acute
upper airway obstruction.
Epidemiology

Most patients with croup are


between ages of 3 mo and 5 yr,
with the peak in the 2nd yr of life.
Prevalence-affects 3-5% of children.
Etiology

The parainfluenza viruses (types


1, 2, & 3) account for ∼75% of
cases.
Other viruses includes influenza
A and B, adenovirus, respiratory
syncytial virus (RSV), and
measles.
Mycoplasma pneumoniae has
rarely been isolated from children
with croup and causes mild
disease.
Pathophysiology
Transmitted via the respiratory
route.
 Initial port of entry is the nose and
nasopharynx.
As the infection spreads distally, so
does the edema causing in
subglottic narrowing.
Begins with a prodrome of a few
days of mild URI with nasal
congestion, sore throat and cough.
Clinical manifestation
Preceding URIs symptoms such
as rhinorrhea, pharyngitis, mild
cough, and low-grade fever for 1-
3 days.
 Then the child develops the
characteristic “barking” cough,
hoarseness, and inspiratory
stridor.
Agitation and crying greatly
aggravate the symptoms and
signs.
Clinical manifestation
Physical examination can reveal
a
 hoarse voice, coryza,
 normal to moderately inflamed
pharynx, and a slightly increased
respiratory rate.
Croup Scoring
0 1 2 3

Stridor None Mild Moderate at Severe on


rest inspiration and
expiration
Retraction None Mild moderate Severe and
marked use of
accessory
muscles
Air entry Normal Mild Moderate marked

Color Normal Normal Normal Dusky or


cyanosis

Level of Normal Restless Anxious, Lethargic &


consciousne when agitated & depressed
ss disturbed restless
score
5 = mild
5-6 = mild to moderate
7-8 = moderate
8 and more = severe
Diagnosis
Croup is a clinical diagnosis and
does not require a radiograph of
the neck.
Radiographs of the neck can
show the typical subglottic
narrowing.
The radiographs do not correlate
well with disease severity.
Treatment
The mainstay of treatment for children with
croup is airway management and treatment
of hypoxia.
Mild croup
Requires only supportive care. Such as:
Antipyretics ,oral hydration, and observation
at home.
Any conditions that may distress the child
should be avoided.
Dexamethasone 0.6 mg/kg IM/IV stat or PO
if able to take.(decrease the edema in the
laryngeal mucosa through their anti-
inflammatory action).
Treatment
Nebulized with epinephrine is an
accepted treatment for moderate or
severe croup.
The mechanism of action is constriction
of the precapillary arterioles causing fluid
resorption from the interstitial space .
Epinephrine by nebulization (0.5ml of
epinephrine mixed with 2.5 saline).
If signs of impending complete airway
obstruction occur ,intubation or
tracheostomy has to done.
Epiglottitis
Epiglottitis is life-threatening
bacterial infection causing
inflammation and edema of the
epiglottis and/or adjacent structures
above the larynx.
• Epidemiology: Occurs in children
from 3-7 yrs in age with only 4%
under the age of 1.
• Etiology :In the past, Haemophilus
influenzae type b was the comment
etiology.

Pathophysiology

Local invasion of the epiglottis occurs


followed by bacteremia.
 The epiglottis, aryepiglottic folds,
false vocal cords, and supraglottic
structures become inflamed and
edematous, leading to narrowed
airway and respiratory compromise.
Inspiratory airway occlusion often
occurs prior to total occlusion from
supraglottic edema.
Clinical manifestation
Is characterized by an acute rapidly
progressive course of high fever, sore
throat, dyspnea, and rapidly progressing
respiratory obstruction.
The patient appears toxic, swallowing is
difficult, and breathing is labored.
Drooling is usually present,
tripod position, sitting upright and
leaning forward with the chin up and
mouth open.
Stridor is a late finding and suggests
near-complete airway obstruction.
Tripod position
Diagnosis
The diagnosis requires visualization of a
large, cherry red, swollen epiglottis by
laryngoscopy.
Laryngoscopy should be performed in
operating room or intensive care unit.
Direct inspection of the oral cavity should
be avoided until the airway is secure.
Cultures of blood, epiglottic surface, can
should be collected after the airway is
stabilized
Classic radiographs of a child who has
epiglottitis show the thumb sign .
Treatment
Epiglottitis is a medical
emergency and warrants
immediate treatment with an
artificial airway.
Ceftriaxone, cefotaxime, or
meropenum should be given
parenterally and continued for 7-
10 days.
Review
Croup Epiglottitis
 Voice – hoarse Voice – muffled
Cough – barking Cough – usually
Fever – yes none
Saliva – minimal Fever – yes

Neck swelling – Saliva – lots


Neck swelling –
little
Begins – slowly lots
Begins – suddenly
Time –
Time-all the day
evening/night
Lower respiratory tract
infections
 Bronchiolitis
 Pneumonia
Bronchiolitis
Introduction

Bronchiolitis, a lower respiratory


tract infection (LRTI) that primarily
affects the small airways
(bronchioles).
Is a common cause of illness and
hospitalization in infants and
young children.
Bronchiolitis is more common in
those who have not been breast-
fed, and in those who live in
Epidemiology

Bronchiolitis typically affects


infants younger than two years.
Has a peak incidence between two
and six months of age.
Bronchiolitis is a leading cause of
hospitalization in infants and
young children up to 5 years of
age.
Etiology
RSV is responsible.
• Other agents include
parainfluenza, adeno virus,
influenza virus and Mycoplasma.
• Emerging pathogens include
human metapneumovirus and
human bocavirus,
Pathophysiology
Viruses infect the epithelial cells
lining the respiratory mucosa
causing direct damage and
inflammation in the small bronchi
and bronchioles.
Acute bronchiolitis is
characterized by bronchiolar
obstruction with edema, mucus,
and cellular debris.
Risk factors
Infantplaced in daycare
Crowded household (more than 4
people in the home)
School age brothers and sisters
Exposure to tobacco smoke
Not breast feeding
Clinical manifestation
The illness begin with URT symptoms and
progress rapidly over 1-2 days to the
development of increased respiratory effort
and wheezing .
Signs and symptoms includes:
Tachypnea, Cough, Irritability, Fever
Poor feeding, Nasal flaring
Episodes of apnea (more common in
infants).
Retractions
Diagnosis
The diagnosis of acute
bronchiolitis is clinical.
Chest radiography can reveal
hyperinflated lungs with patchy
atelectasis.
The white blood cell and
differential counts are usually
normal.
Viral testing (polymerase chain
reaction, rapid
immunofluorescence, or viral
Complication

Apnea
Respiratory failure
Secondary bacterial infection,
mainly otitis media and
secondary bacterial pneumonia
and sepsis are rare.
Treatment
The mainstay of treatment is
supportive.
Hypoxemic children should receive
oxygen.
The infant may be fed through
nasogastric tube.
Frequent suctioning of nasal and oral
secretions often provides relief of
distress.
A trial dose of inhaled bronchodilator
may be reasonable.
Prognosis
The case fatality rate is <1%,
with death attributable to apnea,
respiratory arrest, or severe
dehydration.
pneumonia
Definition and Epidemiology

Pneumonia is inflammation of the


parenchyma of the lungs.
Is a substantial cause of morbidity and
mortality in childhood throughout the world.
≈158 million episodes of pneumonia per
year, of which ≈154 million are occurring in
developing countries.
cause ≈3 million deaths, or an estimated
29% of all deaths, among children younger
than 5 yr worldwide.
The incidence is more than 10-fold higher
and the number of childhood-related deaths
due to pneumonia ≈2000-fold higher, in
developing than in developed countries
Etiology
Most cases of pneumonia are
caused by microorganisms.
noninfectious causes includes:
 aspiration of food or gastric acid,
 foreign bodies
 hydrocarbons
Etiology con’t…
Streptococcus pneumoniae (pneumococcus)
is the commonest pathogen in children 3 wk
to 4 yr of age.
Mycoplasma pneumoniae and
Chlamydophila pneumoniae are the most
frequent in children 5 yr and older.
S. pneumoniae, H. influenzae, and S. aureus
are the major causes of hospitalization and
death among children in developing
countries.
Viral pathogens are a prominent cause of
lower respiratory tract infections in infants
and children <5 yr of age
Etiology con’t…
Influenza virus and respiratory
syncytial virus (RSV) are the major
pathogens, especially in children
<3 yr of age.
Other common viruses include
parainfluenza viruses,
adenoviruses, rhinoviruses, and
human metapneumovirus.
Pathophysiology
Viral pneumonia; spread of infection
along the airways, resulting in direct
injury of the epithelium, airway
obstruction from swelling, abnormal
secretions, and cellular debris.
Bacterial pneumonia occurs when
organisms colonize the trachea and
subsequently gain access to the lungs,
but pneumonia may also result from
direct seeding of lung tissue after
bacteremia.
Pathophysiology con’t…
Immune response leads to
inflammation;
Lung compliance is decreased,
small airways become obstructed
and air space collapse progresses;
Classification
Based on etiology;
 viral, bacterial, fungal
• Based on morphology ;
 bronchopneumonia, lobar pneumonia
and interstitial pneumonia.
• Based on mode of acquiring the
infection;
 community acquired ,hospital acquired
and congenital pneumonia.
• Based on severity;
 sever pneumonia, pneumonia and no
pneumonia
Clinical Manifestations
Viral pneumonias are often preceded
by several days of symptoms of an
URTs.
Tachypnea is the most consistent
clinical manifestation of pneumonia.
Viral pneumonia usually presents with
cough, rhinitis ,fever, increased work
of breathing accompanied by
intercostal, subcostal, and
suprasternal retractions, nasal flaring.
 Auscultation of the chest may reveal
crackles and wheezing.
Clinical Manifestations con’t…
Bacterial pneumonia in adults and older children
typically begins suddenly with a shaking chill
followed by a high fever, cough, and chest pain.
Respiratory distress manifested as grunting;
nasal flaring,retractions of the supraclavicular,
intercostal, and subcostal areas.
Physical findings depend on the stage of
pneumonia which includes diminished breath
sounds, scattered crackles and bronchial breath
sound.
Some infants with bacterial pneumonia may
have associated gastrointestinal disturbances
characterized by vomiting, anorexia & diarrhea.
Diagnosis
Mainly clinical.
In viral pneumonia, the WBC count can be
normal or elevated ,usually not higher than
20,000/mm3, with a lymphocyte
predominance.
Bacterial pneumonia is often associated
with an elevated WBC count, in the range
of 15,000-40,000/mm3, and a
predominance of granulocytes.
An infiltrate on chest radiograph supports
the diagnosis of pneumonia; the film may
also indicate a complication such as a
pleural effusion.
Classification of the severity of
pneumonia
Severe pneumonia
Cough or difficulty in breathing with:
 Oxygen saturation < 90% or central
cyanosis
 Severe respiratory distress (e.g. grunting,
nasal flaring, very severe chest indrawing)
 Signs of pneumonia with a general danger
sign
(inability to breastfeed or
drink, lethargy or reduced
level of consciousness,
convulsions)
pneumonia
Fast breathing:
≥ 50 breaths/min in a
child aged 2–12 months
≥ 40 breaths/min in a child
aged 1–5 years
 Chest indrawing
No pneumonia, cough or cold
 No signs of pneumonia or severe
pneumonia
Common features:
■ cough
■ nasal discharge
■ mouth breathing
■ fever
Treatment
Treatment of suspected bacterial
pneumonia is based on the
presumptive cause and the age and
clinical appearance of the child.
Out patient management options
are; amoxicillin , cefuroxime axetil
and amoxicillin/clavulanate.
 For suspected M. pneumoniae or C.
pneumoniae a macrolide antibiotic
such as azithromycin is an
appropriate choice.
Treatment con’t…
Parenteral cefotaxime or ceftriaxone is
the mainstay of therapy of bacterial
pneumonia in hospital setting.
for staphylococcal pneumonia
(pneumatoceles, empyema), initial
antimicrobial therapy should also
include vancomycin or clindamycin.
If viral pneumonia is suspected, it is
reasonable to withhold antibiotic
therapy.
Supportive care .
Indication for hospitalization
 Age <6 mo
 Multiple lobe involvement
 Immunocompromised state
 Toxic appearance
 Moderate to severe respiratory distress
 Requirement for supplemental oxygen
 Dehydration
 Vomiting or inability to tolerate oral
fluids or medications
 No response to appropriate oral
antibiotic therapy
 Social factors
Childhood
Tuberculosis
Outline
Epidemiology
Etiology
Clinical
features
Diagnosis
Management
Epidemiology
•It is the second leading cause of
death from an infectious disease
worldwide(after HIV)
A third of the world population is
infected with TB
Approximately 95% of tuberculosis
cases occur in the developing
world.
Ethiopia is one of the 22 high
burden countries
In 2015 according to WHO
220,000 new cases of TB and
29,000 deaths were estimated in
Ethiopia
Globally 3.2% of incident cases of
TB( 290,000) are estimated to
have MDR TB
86% of MDR TB burden is carried
in 27 countries
There are three major stages of tuberculosis.
Exposure : that the child has had significant
contact (“shared the air”) with an adult or
adolescent with infectious pulmonary
tuberculosis. Normal TST, CXR and child lacks
symptoms and signs of the disease

Latent infection ( LTBI): occurs after


inhalation of droplet nuclei containing M. TB
◦ characterized by reactive tuberculin skin test and
absence of clinical and radiologic evidence of
active TB.
Tuberculosis disease: occurs when
signs or symptoms or radiologic evidence
of active TB become apparent
 Untreated infants with LTBI have 40%
likelihood of developing disease
compared with only 5-10% in adults
 The greatest risk of progression
occurs during the 1st 2yr after
infection
Etiology
 M. tuberculosis complex: M. tuberculosis, M. bovis, M.
africanum, M. microti, and M. canetti.
 M. tuberculosis is the most important cause of tuberculosis
disease in humans which is:
o Non-spore forming
o Non-motile
o Obligate aerobe
o Slow-growing
o Grow best at 37-41oC
o weakly gram +ve rods
o Cell wall with high lipid content which gives “acid-
fast” staining properties (resistance to decolorization
with acid alcohol)
Transmission
Transmission is person to person (usually by
air borne mucus droplet nuclei)
Risk of transmission is dependent on :
Index case;
Smear positive TB
Copious production of sputum
Severe & forceful cough
Not treated
Environment:

Poor ventilation
Overcrowding
Young children rarely infect others
because:
◦ Sparse bacilli
◦ Cough is often absent or lacks the
tussive force to suspend infectious
particles of correct size
Most adults no longer transmit the
organism within several days to 2
weeks after beginning adequate
chemotherapy
Thetime between initial infection & clinically
apparent disease is variable:
Disseminated & meningeal TB are early
manifestations (2-6mo after infection)
TB LAP & endobronchial TB (3-9mo)
Bones & joints take several years
Renal TB takes decades after infection
 25 to 35% of children with Tbc
develop extrapulmonary
manifestations (10% adult)
 Pulmonary TB that occurs more than a
year after 1o infection is usually due to
endogenous regrowth of bacilli persisting
in partially encapsulated lesions – rare in
children
 Common site of reactivation is the apex
of upper lobes(oxygen & blood flow
good)
Clinical manifestation
General symptoms
 Anorexia
 Night sweat
 Fatigue
 Chronic cough ( > 2 weeks)
dry/producative
 weight loss
 Low grade Fever-remittent(appears late
afternoon & fades out by night)
 Failure to respond to broad spectrum
antibiotics
Progressive pulmonary involvement
 Dyspnea
 Chest tightness
 Mucopurulent sputum
 Hemoptysis
 Chest pain

EXTRA PULUMNORY SYMPTOMS


 Pain
 inflammation
Diagnosis of TB in children
 Acid Fast Staining/culture (sputum, gastric aspirate,LN,
fluid) is definitive
 Smear +ve TB:
The criteria are:
 two or more initial sputum smear examinations
positive for acid fast bacilli; or
 one sputum smear examination positive for
acidfast bacilli plus
 CXR abnormalities consistent with active
pulmonary TB, as determined by a clinician; or
 one sputum smear examination positive for acid
fast bacilli plus sputum culture positive for M.
tuberculosis.
If AFB is negative, Dx is based on:
Contact with patient(adult) with pulmonary
TB
S/Sx suggestive of TB
X-Ray finding consistent with TB
Positive TST
If 3 are fullfilled, TB is likely Dx
Ifsevere malnutrition or immunosupresion, 2
criteria are enough
Management of
childhood TB
Principles :
 Chemotherapy/AntiTB drugs
 Nutritional rehabilitation
 Screening of the family(index case,

other contacts)
 Follow up (Adherence, response,

drug side effects)


Currently Recommended
Antituberculous Regimens

 Short-course chemotherapy (SCC), the


standard current receommendation globally,
is given in two phases, usually for 6 months:
1. Intensive phase

This phase comprises administration of at


least 3 drugs for 2 months to get rid of the
bacterial load and to prevent emergence of
resistant strains of Myc. tuberculosis.
CONT.

2. Continuation phase
◦ This phases comprises
administration of at least 2 drugs
to complete the course, usually for
a period of 4 months.
Treatment Daily dose (mg/kg) and Treatment side effects
Route of administration

Rifampin 10 to 20; Oral Orange body fluids; drug


interactions;
hepatotoxicity;
thrombocytopnea
Isoniazid 5 (preferably as a single Neuropathy;
dose); Oral hepatotoxicity; GI
intolerance
Pyrazinamide 30; Oral Hepatotoxicity; joint
pains; GI intolerance;
hyperuricemia
Ethambutol 15 to 20; Oral Ocular toxicity (dose
related); GI intolerance
Streptomycin 20 to 50; Intramuscular Auditory and vestibular
toxic effects Nephrotoxic
effects; Rash
Ethionamide 15 to 20; Oral Nausea, vomiting,
abdominal pain
Ciprofloxacin 10; Oral Hypersensitivity,
arthralgia
Amikacin 7.5; IV/IM Nephrotoxicity
DOT should be used for all children with
TB.
Streptomycin should be avoided when
possible in children
◦ Injections are painful
◦ Irreversible auditory nerve damage may
occur
9 to 12 months of treatment is required
in the following conditions:
◦ Bone and joint TB
◦ TB meningitis
◦ Miliary TB
2HRZE)/4HR
Drug resistant TB
Mono-resistance: resistance to one anti-
TB drug
Poly-resistance: resistance to one or more
than one anti-TB drug, other than both INH
and R.
MDR TB: TB which is resistance to at least
Rifampicin and INH.
Extensively drug resistance (XDR TB):
MDR TB plus resistance to a fluoroquinolone
and at least to one of the three injectables
(Amikacine, kanamycine and capreomycin)
Diarrheal
Diseases

92
Diarrhea
Definition
The term diarrhea comes from
Greek word "diarrhoia", meaning
to flow through.
Loose stool > 3x/24hrs. (WHO)
An increase in the fluidity, volume
and frequency of stools.
A young infant normally has
~5g/kg of stool output per day.

93
Major causes of mortality
among children under 5
Burden usually severe in less developed
countries; in Ethiopia among the 5 common
killers of under 5 children.
ARI
FACT Perinatal
22%
20%

Malnutrit
ionDiarrhoea
60% 12%

Other
28%
Malaria
8%
Measles
HIV 5%
4%
94
Behavioral risk factors
Environmental factors
◦ Inadeqate breast feeding(first 4-6 months)
◦ Using feeding bottles
◦ Drinking contaminated water
◦ Not washing hands
◦ Eating food hrs after cooking
Host factors
◦ Young age
◦ Malnutrition
◦ Measles
◦ Immunosupression
95
Types Greatest Danger
1. Acute watery Dehydration
diarrhea (80% of K +loss
cases)
2. Bloody diarrhea Tissue damage
(Dysentry) 10% of Toxemia(sepsis)
cases
3. Persistent Malnutrition
diarrhea(> 2 wks)
10% of cases
4. Chronic diarrhea Malnutrition
96
Causative agents of acute
diarrhea
Viral Bacterial Parasites

Rota virus Campaylobactor Giardia


jejuni
Enteric Closteridum E. histolitica
adenovirus defficil and
perfringens
CMV [Link] Cryptosporidium

HSV Shigella and Isospora belli


salmonella
Vibro cholera Strongloidosis

[Link] Trichuris
trichuria
Yersina 97
Mechanisms of
[Link]
Osmotic diarrhea
Defect present:
Digestive enzyme deficiencies
Ingestion of unabsorbable solute
Examples:
Milk  Lactate, small organic acids
Sweetened drinks sucrose, coca cola
Laxative mgso4
Lactase deficiency
Comments:
Stop with fasting, No stool WBCs
98
Mechanisms Cont…
2. Secretory Diarrhea
Defect:
Increased secretion
Decreased absorption(virus
villus damage)
Examples:
Cholera
Toxinogenic [Link]
Comments:
Persists during fasting
No stool leukocytes 99
Mechanisms Cont…
3. Exudative Diarrhea:
Defects:
Inflammation
Decreased colonic
reabsorption
Increased motility
Examples:
Bacterial enteritis
Comments:
Blood, mucus and WBCs
in stool
100
Mechanisms Cont…
[Link] motility:
Defect:
Decreased transit time
Example:
Irritable bowel syndrome, post vagotomy
dumping syndrome

101
Associated Clinical
manifestations
– Fever: may be suggestive of an
inflammatory process.
– Vomiting suggests organisms that
infect the upper intestine (enteric
viruses, enterotoxin- producing
bacteria, Giardia, & cryptosporidium)
– Severe abdominal pain &
tenesmus

102
Assessment of
Diarrhea
—For how long?
—Is there blood in the stool?
—Assess for sign of DHN
—Look at the child’s general condition
—Is the child: Lethargic or
unconscious? Restless and
irritable?
—Look for sunken eyes
—Offer the child fluid. Is the child: Not
able to drink or drinking poorly?
Drinking eagerly, thirsty?
—Pinch the skin of the abdomen. Does
it go back: Very slowly (longer than
2 seconds)? Slowly? 103
Assessment Cont…
 Severe dehydration will have two of these
signs:
◦ Sensorium abnormally sleepy or lethargic
◦ Sunken eyes
◦ Drinking poorly or not at all
◦ Very slow skin pinch
 Some dehydration will have two of these
signs:
◦ Restlessness or irritability
◦ Sunken eyes
◦ Drinking eagerly
◦ Slow skin pinch
 No dehydration
◦ None of these signs 104
Laboratory
Investigation
 CBC
 Stool specimen(mucus, blood,
WBC)
Stool culture: in bloody diarrhea,
WBC positive, and
immunocompromised
 Culture blood
 Serum electrolytes
105
Treatment of diarrhea

Main principle in management of acute


diarrhea is

1. Replace lost water and salts.


2. Continue to feed to prevent
malnutrition(at least 6 times a day).
3. Antibiotics & antiprotozoals when
needed.
4. Prevention of diarrhea.

106
Treatment Cont…
No sign of DHN  Plan A

◦Fluid deficit < 5 %


◦Can be treated at home
◦More fluid than usual to prevent DHN
◦Appropriate supply of foods to prevent
malnutrition
◦Bring back the baby to the health
institution if diarrhea doesn’t get
better or gets worse
107
Home Fluids for Diarrhoea Must Be:
Safe when given in large volume.
Easy to prepare.
Acceptable color and palatability.
HOW MUCH FLUID TO GIVE IN ADDITION TO THE
USUAL FLUID INTAKE:
– Up to 2 years 50 to 100 ml after each loose
stool
– 2 years or more 100 to 200 ml after each loose
stool
 Give frequent small sips from a cup.
 If the child vomits, wait 10 minutes,
continue, but slowly.
 Continue giving extra fluid until the diarrhea
stops.
108
Home Fluids for Diarrhoea Must
Be:
Ideal home fluids contain:
◦salts and nutrients (sodium,
potassium, chloride, and
bicarbonate)
◦calories to replenish diet
Examples of home fluids:
◦ ORS solution
◦ Salted soup
 Rice water
◦ Salted drinks
 Yoghurt drinks 109
Unsuitable fluids
Fluids which are sweetened with
sugar, which can cause osmotic
diarrhoea and hypernatremia
Examples:
Soft
drinks
Sweetened fruit drinks
Sweetened tea

110
Some DHN  Plan B
Fluid deficit 5-10%
ORS 75ml/kg over 4-6 hrs.
Reassess the degree of DHN after 4
hours
◦If no sign of DHN home Rx with
replacement of on going losses
(50-100ml/bowel motion)
◦If sign of some DHN repeat plan B
◦If worse  IV RX
111
Severe DHN  Plan C
Fluid deficit 10-15%
IV fluid RL  30ml/kg in the 1st hr. / 30
min. to combat circulatory collapse for
infant and child respectively.
70ml/kg in the 5hrs/2 ½ hrs. for infant
and child respectively.

112
Zinc supplement
Up to 6 months - 1/2 tablet (10
mg) per day
6 months and more - 1 tablet (20
mg) per day
For 10–14 days

113
Treatment of diarrhea Cont...

Treatment of DHN in malnourished pts


 Whenever possible rehydration should be
PO.
 IVinfusions are very dangerous and not
recommended unless there is severe
shock or loss of consciousness from
confirmed dehydration.
 Malnourished patients tend to develop
electrolyte imbalance with a great excess
of sodium and deficit in potassium.

114
Treatment of diarrhea Cont...
 We use a special ORS for severely
malnourished called ResoMal.
 A total b/n 50-100 ml of Resomal per
kg of body wt. is usually more than
enough to restore normal hydration.
 Give this amount over 12 hrs starting
with 5ml/kg every 30 minutes for the
2 hours orally or by NGT and then 5-
10 ml/kg per hour .
 For each watery stool give 30 ml of
resomal soln.
 115
Treatment of diarrhea Cont...

If the child is in shock and if the child


is unconscious ,then use IV fluids R/L
with 5 % D/W or ½ N/S with 5 % D/W.
Give 15 ml/kg over the 1st hour and
reassess the child. If there is
improvement, repeat the 15 ml/kg IV
over the next hour.
◦ If there is no improvement then assume
that the child has septic shock.
As soon as the child regains
consciousness stop the drip and treat
116
Dysentry
Dysentery is diarrhoea
presenting with loose frequent
stools containing blood
Most episodes are due to Shigella
and nearly all require antibiotic
treatment
DX
◦ Loose stools with visible red blood
◦ Abdominal pain, fever, convulsions,
lethargy, dehydration, rectal
prolapse 117
Treatment
Admission
◦ Children with severe malnutrition and
dysentery
◦ Young infants (<2 months old) with
dysentery
◦ Children who are toxic, lethargic, have
abdominal distension and tenderness or
convulsions
Others can be treated at home
Trt:
◦ Cipro/ceftrioxone for 3 days + prescribe
Zn supplement + prevent or correct
dehydration + continue feeding 118
119
120
Urinary Tract Infections
(UTI)
UTI
Prevalence and Etiology
◦Occur in 4-7% of infants & 3-5% of
school age children with FEVER
◦3-5% of girls and 1% of boys affected
◦In girls average age at first diagnosis
– 3yrs.
◦In boys – first yr of life
◦First year – M:F ratio is 2.8:5.4
◦Beyond 2 yr – M:F ratio is 1:10
◦Mainly caused by colonic bacteria
◦ In females 75-90% caused by E. coli
followed by Klebsiella and proteus
◦ In males > 1 yr proteus is as common
as E. coli
◦ Other causes are viral (adenovirus) –
especially in cystitis
Classification
◦ Three basic forms
 Pyelonephritis
 Cystitis
 Asymptomatic Bacteriuria
Pyelonephritis
◦Manifests with any or all of the
following:
 Abdominal or flank pain, fever,
malaise, vomiting.
 Some newborns may show non
specific symptoms such as poor
feeding, irritability and weight loss
◦Acute form may result in renal
scarring
Cystitis
◦Indicate bladder involvement, and
manifest:
Pathogenesis
◦ Ascending infection from fecal flora
◦ Rarely hematogenous
◦ Infected urine gets to intra-renal area ➞
inflammatory response ➞ renal injury
and scarring
Risk
Factors
Female Tight underwear
Uncircumcised male Pinworm infestation
Vesico-urethral Anatomic
reflux abnormalities
Toilet training Neurogenic bladder
Voiding dysfunction Sexual activities
Obstructive
uropathy
Urethral
instrumentation
Wiping from back to
front
Bubble bath
Diagnosis
Urineculture; depends on having
proper urine sample:
◦ In toilet trained children
 Mid-stream urine
 If > 100,000 colonies of a single
pathogen or
 If 10,000 colonies and child is
symptomatic ~ UTI
UTI…
◦ In infants
 Sterile collection bag after skin disinfection
may help to avoid contamination
 Symptoms + > 100,000 colonies ~ Presumed
UTI
 If above is not possible, catheterization
needed for urine collection
 Urinalysis
 Pyuria (leucocytes in urine) suggests
infection,
UTI…
 Positive Nitrites and leukocyte esterase
 WBC casts
Hematology
 Leucocytosis, neutrophilia, elevated ESR
and CRP are common
Treatment
◦ Acute cystitis
 Trimethoprim – Sulfamethoxazole or
 Nitrofurantoin or
 Amoxicillin for 5 days
AFI suggestive of Pyelonephritis
 Ceftriaxone or
 Ampicillin + Aminoglycoside for 10-14
days
Meningitis beyond the neonatal age
Introduction
Meningitis refers to inflammation of
the leptomeninges, the connective
tissue layers in closest proximity to
the surface of the brain.
In general, viruses > bacteria > fungi
> parasites, in terms of causing CNS
infections.
BACTERIAL
MENINGITIS
Etiologies
 Common etiologies of acute bacterial meningitis
= S pneumoniae = H influenzae =N
meningitidis

 Uncommon etiologies of acute bacterial


meningitis

= P aeruginosa = S aureus =
Salmonella spp
= L monocytogenes = Coag neg
Staphylococcus
General risk factors
Lack of immunity associated with
young age.
Infants & young children with
occult bacteremia
Responsible serotypes

N meningitidis

Sero-groups A, B, C, W135 & Y (out of the 13


groups)

H influenzae Type B (out of the 6 groups)

* Epidemiology may have changed since the


introduction
of the Hib vaccine
Pathogenesis
Bacterial colonization of nasopharynx
Attach to mucosal epith.
cell receptors by pili

Breach mucosa & enter circulation


Large capsules interfere
with phagocytosis
To CSF through choroid
plexus of ventricles
Extra-cerebral CSF &
Sub-arachnoid space
Bacterial proliferation

Inflammation-cytokines
Clinical features
 Nonspecific SSx - fever, poor feeding, headache, URTI SSx,
myalgias, arthralgias

 Tachycardia, hypotension, and cutaneous signs, such as


petechiae,
purpura, or erythematous macular rash (meningococcemia)

 Meningeal signs - more likely to be observed in older


children
 Nuchal rigidity,
 Kernig sign (flexion of hip 90o followed by pain with leg
extension,
 Brudzinski sign (involuntary flexion of knees & hips after
passive
flexion of the neck while supine).
Clinical features & associated
pathologies
 Headache, emesis, bulging fontanel or diastasis
(widening)
of the sutures, CN 3 or 6 paralysis, hypertension with
bradycardia, apnea or hyperventilation, decorticate or
decerebrate posturing, stupor, coma … Raised ICP

 Cranial
neuropathies (CN 2, 3, 6, 7, 8) … Focal
inflammation

 Seizures

 Altered
mental status … Raised ICP,
hypotension/cerebritis
Diagnosis

 CSF analysis and culture

 Bloodcultures (positive in 80% to 90% of


cases)

* When you need to evaluate complications

 Neuro-imaging (Brain U/S, CT, MRI)

 Urinalysis and serum sodium


Lumbar puncture
INDICATIONS

 To diagnose central nervous system (CNS)


infections
 To monitor efficacy of antimicrobial therapy in
CNS infection
 To drain CSF in communicating hydrocephalus
associated
with intraventricular hemorrhage
 To diagnose intracranial hemorrhage
 To diagnose CNS involvement with leukemia
 To inject chemotherapeutic agents
Lumbar puncture

CONTRAINDICATIONS

 Increased intracranial pressure (ICP)


 Uncorrected thrombocytopenia or bleeding diathesis
 Infection in the skin or underlying tissue at or near
the
puncture site
 Lumbosacral anomalies
 Cardiorespiratory instability, which may be
exacerbated by
the procedure
CSF analysis
 Inbacterial meningitis, CSF shows  pressure, 
protein (BBB inflammation),  glucose (partly
resulting from its consumption as a bacterial
nutrient), and many neutrophils.

* turbid/frank pus – a minimum of 200


cells/mm3
Form of Opening WBCs & Protein Glucose Comments
meningitis pressure differential

Normal 50 - 80 < 5, >75% 20 - 45 > 50


values mm H2O lymphocyt mg/dl mg/dl
es
Acute Usually  Usually Usually Usually Organisms
bacterial (100 to 300 – 100 – < usually
meningitis 300) 2,000; 500 40 seen on
PMNs Gram stain
predominat / culture
e
Partially Normal 5 – 10,000; Usually Normal
treat-ed or PMNs usual 100 – or
bacterial elevated 500 decrease
meningitis d
Viral Normal Rarely Usually Generally
meningitis or >1,000 50 – normal
slightly  cells. 200
(80 – Mono-
150) nuclear
cells
Principles of treatment

 IV antibiotics as soon as the LP is done

 IV
antibiotics as soon as possible if there are
contraindications for LP; then do a CT scan

 Treat raised ICP and seizures (if present)

 IVdexamethasone QID for 2 days (for those


older than 6 wks of age) - give 1-2 hr before
antibiotics are initiated or concurrently with the
1st dose of antibiotics.
Recommended empirical therapy
Vancomycin(60mg/kg/24hr,given q 6hr) +
cefotaxime(200mg/kg/24hr,given q 6hr)
or
ceftriaxone(100mg/kg/24hr,given q12hr)
Immunocomp. & suspected gram neg.

ceftazidime/aminoglycoside added
Duration
◦ [Link]- 10-14 days
◦ HIB- 7-10 days
◦ [Link]- 5-7 days

14
Acute complications
 Seizures
 Raised ICP
 Cranial nerve palsies
 Stroke
 Cerebral or cerebellar herniations
 Thrombosis of the dural venous sinuses
 Subdural effusion
 Ventriculitis with hydrocephalus
Chronic complications

 Visualimpairment
 Sensorineural hearing loss
 Behavioral problems
 Cognitive dysfunction
 Recurrent seizures

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