PEDIATRICS II​ L​ ecturer: dr rodolfo ng 

S1-04b: Bacterial infections part 1b​ Date: 10-06-2020

OUTLINE
○ 📣 ​Properdin is very important in complement
reaction or response
● Risk is also increased in patients with ​nephrotic
syndrome, systemic lupus erythematosus
I. Vaccine-preventable Bacterial Infections
(SLE), and hepatic failure and in ​patients
A. Neisseria meningitidis (Meningococcus)
treated with eculizumab​, a monoclonal antibody
a. Etiology
against complement protein C5 (with acquired
b. Epidemiology
complement deficiency).
c. Pathophysiology
d. Clinical Manifestations
e. Diagnosis
b. 📖 ​Epidemiology
f. Treatment
● Transmitted during close contact through ​aerosol
g. Complications
droplets or exposure to respiratory secretions
h. Prognosis
(ex. kissing)
i. Prevention
● The organism does not survive for long periods in
II. Dermatologic-associated Bacterial Infections
the environment.
A. Mycobacterium leprae (Leprosy or
● Enhanced rates of mucosal colonization and
Hansen's Disease
increased disease risk are associated with
a. Etiology
activities that increase the likelihood of exposure
b. Epidemiology
to a new strain or increase proximity to a carrier,
c. Pathophysiology
thus facilitating transmission including:
d. Clinical Manifestation
○ Kissing
e. Diagnosis
○ Bar Patronage
f. Treatment
○ Binge Drinking
g. Long-term Complications
○ Attendance at nightclubs
h. Prevention
○ Living in dormitories
III. Post Quiz
● Factors that damage the nasopharyngeal mucosa
such as smoking and respiratory viral infection
References: Lecture Recording, Powerpoint
(notably influenza) are also associated with
Presentation, and Nelson Textbook of Pediatrics, 20th
increased rates of carriage and disease
ed.
○ By driving upregulation of host adhesion
molecules that are receptors for
📖
Legend:

📣 Reference textbook
●
meningococci.
Carriage is unusual in early childhood and peaks
💡 Audio from lecture recording
Nice-to-Know
⭐ TG Notes
●
during adolescence and young adulthood.
The highest rate of meningococcal disease
occurs in infants younger than 1 yr old​,
probably as a result of:
VACCINE-PREVENTABLE BACTERIAL INFECTIONS ○ Immunologic inexperience - antibody that
recognizes meningococcal antigens is
naturally acquired during later childhood
Neisseria meningitidis ○ Immaturity of the alternative and lectin
complement pathways
○ Perhaps the poor responses made by infants
a. Etiology to bacterial polysaccharides.

● ​ r the meningococcus is a
Neisseria meningitidis o
gram-negative, fastidious, encapsulated,
oxidase- positive, and aerobic​ d​ i​plococcus
● Incubation period: 1-14 days
● Individuals with inherited deficiencies of
Properdin, factor D, or terminal complement
components have up to a 1,000-fold higher risk
for development of meningococcal disease than
complement-sufficient people.
c. 📖 ​Pathogenesis & Pathophysiology
WARNING: This portion is text-heavy due to the
extensive details and step by step explanation
provided by the book.
[This part was not included in the ppt so this could
serve as a supplementary reading (​High-yield siya so
read niyo kapag may time​)]

7RANS FORMERS 1

● Colonization of the nasopharynx by ​N.
meningitidis is the first step in either carriage
or invasive disease.
● Disease usually occurs 1-14 days after acquisition
of the pathogen.
● Initial contact of meningococci with host epithelial
cells is mediated by pili, which may interact with
the host ​CD46 molecule or an integrin​.
● Close adhesion is then mediated by ​Opa and
Opc binding to ​carcinoembryonic antigen cell
adhesion molecule receptors and integrins​,
respectively
● Subsequent internalization of meningococci by
epithelial cells is followed by transcytosis (to the
basolateral tissues) and dissemination into the
bloodstream ​Immunoglobulin A1 protease
secreted by invasive bacteria degrades
secretory immunoglobulin A on the mucosal
surface, circumventing this first-line host defense
mechanism.
● Once in the bloodstream, meningococci multiply
rapidly to high levels to cause septicemia.
● Patients with a higher bacterial load have a
more rapid clinical deterioration and longer
period of hospitalization, ​as well as a ​higher
risk of death​ and ​permanent sequelae.
● Resistance to complement-mediated lysis and
phagocytosis is largely mediated by the
polysaccharide capsule and
lipopolysaccharide (LPS)
○ Outer membrane vesicle blebs released from
the surface of the organism contain LPS,
outer membrane proteins, periplasmic
proteins, and phospholipid, and play a major
role in the inflammatory cascade that leads to
severe disease.
○ Much of the tissue damage is caused by host
immune mechanisms activated by LPS.
○ During invasive disease LPS is bound to a
plasma protein: ​LPS binding protein​.
○ The host receptor complex for LPS consists of
toll-like receptor 4, CD14, and myeloid
differentiation protein 2.
○ Binding of LPS to toll-like receptor 4​, which
is upregulated on circulating leukocytes
during septicemia, results in activation of a
number of different cell types.
○ An intense inflammatory reaction ensues due
to the secretion of pro-inflammatory cytokines
such as ​tumor necrosis factor-α,
interleukin (IL)-1β, IL-6, IL-8, and
granulocyte macrophage
colony-stimulating factor​, levels of which
are closely associated with plasma levels of
LPS.
○ The ​major antiinflammatory cytokines
IL-1Ra, IL-2, IL-4, and IL-12. ​and
transforming growth factor-β are ​present
at very low levels.
● Both high and low levels have been observed for
IL-10 and interferon-γ.
7RANS FORMERS
S1-04b: bacterial infections part 1b
● The pathophysiologic events that occur during
meningococcal septicemia are largely related to
microvascular injury leading to:
○ Increased vascular permeability and the
capillary leak syndrome
■ Increased vascular permeability can lead
to dramatic fluid loss and severe
hypovolemia.
■ Capillary leak syndrome with or without
aggressive fluid resuscitation (which is
essential in severe cases) leads to
pulmonary edema and respiratory failure.
○ Pathologic vasoconstriction and
vasodilation
■ Initial vasoconstriction is a compensatory
mechanism in response to hypovolemia
and results in the clinical features of pallor
and cold extremities.
■ Following resuscitation, some patients
experience “warm shock,” that is, intense
vasodilation with bounding pulses and
warm extremities, despite persistent
hypotension and metabolic acidosis.
○ Disseminated intravascular coagulation
■ Virtually all antithrombotic mechanisms
appear to be dysfunctional during
meningococcal sepsis, leading to a
procoagulant state and disseminated
intravascular coagulation.
○ Profound myocardial dysfunction
■ All of these factors contribute to
depressed myocardial function, but there
is also a direct negative cytokine effect on
myocardial contractility, thought to be
largely mediated via IL-6.
■ Hypoxia, acidosis, hypoglycemia,
hypokalemia, hypocalcemia, and
hypophosphatemia are all common in
severe septicemia and further depress
cardiac function.
■ Some patients become unresponsive to
the positive inotropic effects of
catecholamines and require high levels of
inotropic support during intensive care
management.
● These processes result in impairment of
microvascular blood flow throughout the body and
ultimately lead to multiorgan failure, which is
responsible for much of the mortality.
● Following invasion of the circulation,
meningococci may also penetrate the blood–brain
barrier and enter the cerebrospinal fluid (CSF),
facilitated by pili and possibly Opc.
● Once there, bacteria continue to proliferate and
LPS and other outer membrane products can
stimulate a proinflammatory cascade similar to
that observed in the blood.
○ This leads to upregulation of specific
adhesion molecules and recruitment of
leukocytes into the CSF.
● Central nervous system damage occurs directly
by meningeal inflammation and indirectly by
2
 S1-04b: bacterial infections part 1b
circulatory collapse and causes a high rate of
neurologic sequelae in affected patients.
● Death can occur from cerebral edema, which
leads to raised intracranial pressure and cerebral
or cerebellar herniation.

d. Clinical Manifestations

● The ​most common form of meningococcal

infection is ​asymptomatic carriage of the
organism ​in the nasopharynx​.
● Highest proportion of cases present with
meningococcal meningitis (30–50%).
● Other recognized presentations include
bacteremia without sepsis, meningococcal
septicemia with or without meningitis, pneumonia,
chronic meningococcemia, and occult bacteremia
● Focal infections in various sites (e.g.,
myocardium, joints, pericardium, bone, eye,
peritoneum, sinuses, middle ear) are well
recognized, and all may progress to disseminated
disease
● Urethritis, cervicitis, vulvovaginitis, orchitis, and
Figure 2 ​Purpura
● In fulminant meningococcal septicemia, the
disease progresses rapidly over several hours
from fever with nonspecific signs to septic
shock characterized by prominent petechiae and
purpura (purpura fulminans) with poor peripheral
perfusion, tachycardia (initially to compensate for
reduced blood volume resulting from capillary
leak), increased respiratory rate (to compensate
for pulmonary edema), hypotension (a late sign of
shock in young children), confusion, and coma

●
proctitis may also occur.
Nonspecific early symptoms of acute ● 📣
(resulting from decreased cerebral perfusion).
​For a patient with shock, they do not
immediately cause hypotension. When you see a
meningococcal septicemia include fever,
irritability, lethargy, respiratory symptoms, refusal patient whose blood pressure is reduced, that is
to drink, and vomiting. rather a late sign. So if that happens, you really
● Less frequently, diarrhea, sore throat, and have to put in extra effort because chances are,
chills/shivering are reported your patient is already in a bad shape.
● A maculo-papular rash is evident in
approximately 10% of cases early in the

● 📣
course of infection
​So in the presence of fever, and if for example
at the start you thought that the patient is not
toxic, you might mistake this for viral exanthem or
viral infection
● Limb pain, myalgia, or refusal to walk may occur
as the primary complaint in 7% of otherwise

● 📣
clinically unsuspected cases
​Refusal to walk is understandably due to the
limb pain or muscle pain
● As disease progresses, cold hands or feet and
abnormal skin color may be important signs,
📣
​ urpura Fulminans ( Gangrene na, when you see a
Figure 3 P
patient like this, chances are that the prognosis for survival
capillary refill time becomes prolonged, and a ​non would be very, very poor)
blanching or petechial rash will develop in
>80% of cases​. ● Coagulopathy, electrolyte disturbance (especially
hypokalemia), acidosis, adrenal hemorrhage,
renal failure, and myocardial failure may all

● 📣
develop.
​Itong acidosis, it can be metabolic initially, and
then if the condition deteriorates you can have
both metabolic and respiratory acidosis.
● Meningitis may be present

e. Signs and Symptoms

​ on-blanching or Petechial Rash

Figure 1 N ● Nonspecific S/S of Meningococcal meningitis:
○ Fever and headache, predominate, especially
in the young and early in the illness.

○ 📣
○ Children <5 yr old rarely report headache.
​You can see that the initial signs and
symptoms are nonspecific.

7RANS FORMERS 3

● More specific symptoms:
○ Photophobia
○ Nuchal rigidity
○ Bulging of the fontanel (for infants)
○ Clinical signs of meningeal irritation may
■ 📣
develop but are unusual in infants.
​Meningeal irritation is not very
prominent in children less than 2 years
old
● Seizures and focal neurologic signs occur less
frequently
● A meningoencephalitis-like picture can occur,
associated with rapidly progressive cerebral
edema and death from increased ICP, which may
be more common with ​capsular group A
infection​.
● Occult meningococcal bacteremia manifests as
fever with or without associated symptoms that
● 📣
suggest a minor viral infection.
​This tells us that meningococcal infection can
occur with only fever as its only manifestation
● Resolution of bacteremia may occur without
antibiotics, but sustained bacteremia leads to
meningitis in approximately 60% of cases and to
distant infection of other tissues.
● Chronic meningococcemia, which occurs rarely, is
characterized by:
○ Fever
○ Non-toxic appearance
○ Arthralgia
○ Headache
○ Splenomegaly
○ A maculopapular or petechial rash
●
●
📣
Symptoms are intermittent, with a ​mean duration
of illness of 6-8 wk ​( ​take note)
may spontaneously resolve, but meningitis may
develop in untreated cases.
f. Diagnosis
● Variable: leukocytopenia or leukocytosis, often
with increased percentages of neutrophils and
band forms, and anemia, thrombocytopenia,
proteinuria, and hematuria.
● Elevations of erythrocyte sedimentation rate
(ESR) and C-reactive protein (CRP) may occur,
but in patients with rapid onset of disease, these
● 📣
values may be within normal limits at presentation
​elevation of ESR & CRP are non-specific; they
are inflammatory markers
● Increased CRP in the presence of fever and
petechiae makes the diagnosis likely.
● Common in patients with meningococcal
septicemia:
○ Hypoalbuminemia
○ Hypocalcemia
○ Hypokalemia
○ Hypomagnesemia
○ Hypophosphatemia
○ Hypoglycemia
○ Metabolic acidosis, often with increased
lactate levels
7RANS FORMERS
S1-04b: bacterial infections part 1b
■ 📣 ​Could be due to shock or poor tissue
perfusion.​ ​Lactate level can also be used
as a septic marker
● Patients with coagulopathy have decreased
serum concentrations of prothrombin and
○ 📣
fibrinogen and prolonged coagulation times.
​Watch out because pt may develop
bleeding
● Isolation of N. meningitidis from a normally sterile
body fluid such as blood, CSF, or synovial fluid.
● Blood culture may be positive in more than two
thirds of cases before antibiotic use, culture
results often are negative if the patient has been
treated with antibiotics prior to collection of the
culture specimen;
● PCR using whole blood has high sensitivity and
specificity for detection of meningococci
● CSF findings will be that of an acute bacterial
meningitis in meningococcal meningitis
g. Treatment
● Third generation cephalosporins:
○ Cefotaxime or ceftriaxone
■ Unless In regions with a high rate of
β-lactam–resistant S. pneumoniae; if so,
empirical addition of intravenous (IV)
vancomycin is recommended
● Supportive care:
○ Supplemental oxygen for hypoxia
○ Volume replacement
○ Inotropic support for hypovolemia
○ Corticosteroids
■ But recommend replacement doses of
corticosteroids in patients with
treatment-refractory septic shock, since
severe sepsis caused by meningococcus
is associated with adrenal insufficiency
resulting from adrenal necrosis or
hemorrhage (Waterhouse-Friderichsen
syndrome)
h. Complications
● Adrenal hemorrhage, endophthalmitis, arthritis,
endocarditis, pericarditis, myocarditis, pneumonia,
lung abscess, peritonitis, and renal infarcts can
●
occur during acute infection.
Renal insufficiency requiring dialysis may result
from prerenal failure.
● Reactivation of latent herpes simplex virus
infections is common during meningococcal
infection
● The ​most common complication of acute
severe meningococcal septicemia is focal skin
infarction​, which typically ​affects the lower
limbs and can lead to substantial scarring and
require skin grafting.
● Distal tissue necrosis in purpura fulminans may
require amputation (which should be delayed to
allow demarcation) in approximately 2% of
survivors.
4

● Deafness is the most frequent neurologic
sequelae of meningitis​, occurring in 5–10% of
○ 📣
children.
​Unlike in H. influenzae, you do not give
early corticosteroids to prevent deafness. You
administer corticosteroids if the sepsis or
meningitis is severe.
○ Cerebral arterial or venous thrombosis with
resultant cerebral infarction can occur in
severe cases.
● Behavioral and psychosocial complications of the
disease are frequently reported.
i. Prognosis
● Poor prognostic factors on presentation include
hypothermia or extreme hyperpyrexia,
hypotension or shock, purpura fulminans,
seizures, leukopenia, thrombocytopenia (including
DIC), acidosis, and high circulating levels of
endotoxin and TNF-α.
● The presence of petechiae for <12 hr before
admission, absence of meningitis, and low or
normal ESR indicate rapid, fulminant progression
and poorer prognosis
j. Prophylaxis
● Household contact prophylaxis is require
especially in children <2 yr old
● Childcare or preschool contact at any time during
7 days before onset of illness
● Direct exposure to index patient's secretions
through kissing, sharing toothbrushes or eating
utensils at any time during 7 days before onset of
illness
● Mouth-to-mouth resuscitation, unprotected
contact during endotracheal intubation during 7
days before the onset of illness
○ Frequently slept in same dwelling as index
patient during 7 days before onset of illness
○ Passengers seated directly next to the index
case during airline flights lasting >8 hr
● Ceftriaxone and ciprofloxacin are the most
effective agents for prophylaxis, with ciprofloxacin
●
the drug of choice in some countries.
Rifampin is most widely used but fails to eradicate
colonization in 15% of cases
k. Vaccination
● 📣 ​Conjugate vaccine can be given to a child as
young as 2 mos., but there are some where the
● 📣
youngest you can give is at 9 mos.
​Meningococcal vaccine has never been
considered as a selective vaccine. This vaccine is
among the routine vaccines, therefore it is
mandatory.
● Tetravalent meningococcal (ACYW-135)
conjugate vaccine MC4-D, MCV4-TT, MCV4-CRM
(IM)
7RANS FORMERS
S1-04b: bacterial infections part 1b
● Tetravalent meningococcal polysaccharide
vaccine (MPSV4) given IM/SC)
● MCV4-D​:
○ Minimum age is 9 months.
○ For children 9-23 months, give 2 doses 3
months apart
○ For children 2 years and above, give one
dose, except in cases of asplenia, HIV and
persistent complement component deficiency
where 2 doses, 8 weeks apart are
recommended.
● MCV4-TT
○ Given to children 12 months and above as a
single dose
● MCV4-CRM given to children 2 years and above
as a single dose
●
📣
Indicated for those at high risk for invasive
disease: (
vaccine)
But can be given as a routine
○ Persistent complement component
deficiencies (including those with inherited or
chronic deficiencies in C3, C5-9, properdin,
factor D, factor H)
○ Anatomic/ functional asplenia (including sickle
cell disease)
○ HIV
○ Travelers to or resident of areas where
meningococcal disease is hyperendemic or
epidemic, including countries in the African
meningitis belt or the Hajj, or belonging to a
defined risk group during a community or
institutional meningococcal outbreak
DERMATOLOGIC-ASSOCIATED BACTERIAL INFECTIONS
Mycobacterium leprae
a. Etiology
● Mycobacterium leprae -​ an obligate intracellular
acid-fast, Gram-positive bacillus of the family
Mycobacteriaceae m ​ easuring 1-8 μm in length.
●
cells of peripheral nerves ​( 📣
The only bacterium known to infect Schwann
difference from
other Mycobacterium). Identification of acid-fast
bacilli in peripheral nerves if pathognomonic of
leprosy.
● The exact mechanism of transmission is not fully
primarily by the ​respiratory route ​(
breathing, inhale)
📣
understood but is thought to occur ​(REMEMBER!)
coughing,
● The incubation period between natural infection
and overt clinical disease in humans ranges from
3 mo to 20 yr, with a mean of ​4 yr for
tuberculoid leprosy and 10 yr for lepromatous
leprosy​. Most cases are not diagnosed until
● 📣
several years after initial exposure.
Many cases are not diagnosed because of
prolonged incubation period
5

b. 📖 ​Epidemiology
● Approximately 245,000 new cases were reported
globally in 2009, with more than 80% of cases
occurring in Southeast Asia, Africa, and South
America.
● infection in infants is rare, the youngest patient
reported in the literature is a 3 mo old.
● The likelihood of developing HD is determined by
several variables:
○ age (with 2 incidence peaks: 10-14 yr and 30
yr),
○ gender (male :female 2 : 1), and
○ contact with a patient with multibacillary
disease.
● Approximately 5% of people are genetically
susceptible to infection with M. leprae.
● Type of disease (multibacillary) and proximity to
contact cases are important determinants of
human-to-human transmission; the relative risk for
developing disease in household contacts is 8-10
for lepromatous disease and 2-4 for the
tuberculoid form.
c. 📖 ​Pathophysiology
● The dissemination from the respiratory tract to the
skin and nerves is thought to occur
hematogenously but has not been completely
elucidated.
● ​M. leprae ​colonize the perineural space and gain
entry into the endoneural space
● binds to the laminin-2 glycoprotein present in the
basal lamina of Schwann cells in peripheral
nerves
● taken up inside the Schwann cell, where it
replicates slowly intracellularly over several years
● the immune response to infection also contributes
to nerve damage
● Schwann cells express human leukocyte antigen
class 2 molecules that present mycobacterial
peptides to the human leukocyte antigen class
2–restricted CD4-positive T cells. This likely
explains the nerve damage seen in paucibacillary
disease and in reversal reactions.
d. Clinical Manifestations
● The hallmark clinical findings in leprosy are
📣
hypopigmented skin lesions with loss of
sensation​. ( This is very important! People
● 📣
with vitiligo should be careful)
What differentiate one from the other is the
loss of sensation or what we call ​hypoesthesia ​or
○ 📣
anaesthesia
If you are going to do pricking with a
needle on the site of hypopigmented skin
lesion:
■ Normal with intact peripheral nerves -
pain sensation
■ HD - no pain sensation
● These lesions are observed more frequently in the
cooler areas of the body, such as the ​nose and
the ​earlobes
7RANS FORMERS
S1-04b: bacterial infections part 1b
● Hypoesthesia is the clinical manifestation of
peripheral nerve involvement and is present in as
many as 70% of children with this condition. (
30% will not show this manifestation)
📣
● Depending on the number of lesions and the
number of bacilli observed on the lesion’s smear,
leprosy can be classified into the following 3
groups:
○ Paucibacillary (PB) or tuberculoid (TT)
leprosy
■ TT leprosy presents with one or few
(usually <5) hypopigmented and
hypoesthetic lesions. Sensory loss is
frequently observed around the lesions
■ Patients with tuberculoid leprosy have a
characteristic normal
response to ​M. l​ ​eprae ​antigens. (
They can react to Tuberculin testing but
📣
cell-mediated
Ex.
not necessarily secondary to TB)
Figure 4​ A patient with tuberculous leprosy with a single skin
lesion with a raised border and flattened center. P. 1462,
Nelson’s Textbook of Pediatrics, 20th ed.
○ Multibacillary (MB) or lepromatous (LL)
leprosy
■ usually presents with multiple (>5) poorly
defined, hypopigmented or erythematous
lesions associated with hypoesthesia.
■ It is also associated with the presence of
papules, macules, and nodular lesions.
Necrotizing erythema nodosum (rarely)
has occasionally been reported in children
■ Patients with advanced LL leprosy may
present with ​loss of ​eyelashes or
eyebrows and nasal septum
perforation.
■ The constellation of disfiguring facial
📣
features associated with this disease is
named ​“Leonine facies”. - ​
particular
​very
■ The peripheral neuropathy observed in LL
leprosy causes muscle weakness and
atrophy and has been associated with
claw hands and foot drops.
■ Other clinical manifestations of LL leprosy
include corneal opacifications, keratitis,
iritis, testicular atrophy, and kidney
disease resulting in renal failure. Patients
with LL leprosy present with
characteristically abnormal cell-mediated
responses to ​M leprae​ antigens.
6

■ 📣 There are varied manifestation
affecting the eye - ​REMEMBER: eyes is
one of the area that is cool
■ Erythema nodosum leprosum (ENL) is a
borderline and LL leprosy. ( 📣
condition observed in patients with
The term
implies a nodule so you can palpate a
mass)
■ It is usually associated with neuritis, fever,
and arthralgias.
■ The development of ENL has been
suggested to be caused by the presence
of immune complexes
○
■ 📣
Borderline leprosy
​between Paucibacillary and
Multibacillary
■ characterized by the presence of single or
area​. - 📣
multiple skin lesions with a raised central
would appear like a mass
■ It is often subclassified as borderline
tuberculoid (BT), mid borderline (BB), and
borderline lepromatous (BL).
Figure 5 ​A patient with borderline leprosy with numerous,
hypopigmented lesions with poorly defined borders. P. 1463,
Nelson Textbook of Pediatrics, 20th ed.
e. ​Diagnosis
● M. leprae​ cannot be cultured in vivo
● Full-thickness skin biopsy and PCR are the main
laboratory tests to aid in the diagnosis
● Patients are considered to have HD if they have 1
or more of the 3 cardinal signs:
○ loss of sensation​ in a localized skin lesion,
○ thickened peripheral nerve with loss of
sensation or weakness of muscles innervated
by that nerve, or
○ the ​presence of acid-fast bacilli (AFB) on
biopsy​.
● The positive predictive value for the diagnosis of
leprosy in patients meeting all 3 criteria is 98%.
● Histopathologic examination of full-thickness
biopsies taken of active lesions is considered the
gold standard for establishing the diagnosis and
allows for precise disease classification.
f. Treatment
● The primary goal of treatment is early antimicrobial
therapy to prevent permanent neuropathy. Leprosy
is curable.
● Effective treatment requires multidrug therapy
(MDT) with dapsone , clofazimine , and rifampin .
7RANS FORMERS
S1-04b: bacterial infections part 1b
● Combination therapy is employed to prevent
antimicrobial resistance.
Table 1​ World Health Organization Recommended Multidrug
Therapy Regimens for Hansen Disease, p.1464, Nelson
Textbook of Pediatrics, 20th ed. (See appendix)
💡
● In children younger than 10 yr of age, dosages
of multidrug therapy should be in mg/kg, not to
exceed the adult daily maximum: rifampicin 10
mg/kg once monthly, dapsone 2 mg/kg/day,
📖
clofazimine 1 mg/kg on alternate days.
● Before starting combination MDT, patients
should be tested for ​glucose-6-phosphate
dehydrogenase deficiency, have a ​baseline
complete blood cell count and liver function
testin​g, and be ​evaluated for evidence of
concomitant tuberculosis infection. The latter is
imperative so as to avoid giving rifampin
● 📖
monotherapy to someone with active tuberculosis.
​Darkening of the skin is a common adverse
reaction to clofazimine; this generally resolves
6-12 mo after completing therapy.
● Bone marrow suppression and hepatotoxicity
have been reported and should be monitored
every 3 mo during therapy.
● Yearly, a screening urinalysis should be
performed.
● Response to therapy:
○ flattening or disappearance of skin lesions;
○ improvement in nerve function, usually within
1-2 mo after initiating MDT.
○ Complete resolution or improvement may take
6-12 mo, depending on the severity of
infection.
○ Most skin lesions heal without scarring. A
large number of dead bacilli may remain in the
tissue for years before they are eliminated.
○ After completion of MDT, annual follow up for
≥5 yr for paucibacillary and ≥10 yr for
multibacillary disease is warranted.
📖
g. ​Long-term Complications
● Leprosy is a leading cause of permanent physical
disability among communicable diseases
worldwide.
● The major chronic complications and deformities of
leprosy are caused by ​segmental demyelination
and ​permanent nerve injury.
● Nerve impairment may be purely sensory, motor,
or autonomic, or may be a combination.
○ Sensory deficits lead to undetected trauma,
ulceration, and osteomyelitis.
○ Motor deficits ​result in muscle paralysis,
atrophy, and limb deformities, especially of
7

small muscles of the hand and foot (claw hand
or foot, foot drop).
○ Autonomic deficits can lead to skin drying
and cracking.
○ The most chronic residual deformity is that of
an insensitive foot and requires frequent,
routine surveillance of the plantar aspect of
both feet.
○ Patients at highest risk of nerve impairment
are those with multibacillary leprosy and
preexisting nerve damage.
○ An ophthalmologist should routinely examine
all patients with HD because ocular
complications, such as lagophthalmos and
blindness, can occur.
S1-04b: bacterial infections part 1b
a. The most common meningococcal infection is
the asymptomatic carriage of the organism in
the nasopharynx
b. Corticosteroids must always be administered in
a meningococcemia patient to avoid deafness
c. Normal ESR and CRP levels are present in a
meningococcal infection
d. Nonspecific early symptoms of acute
meningococcal septicemia include fever,
irritability, lethargy, respiratory symptoms,
refusal to drink, and vomiting.
5. As a meningococcal disease progresses, cold
hands or feet and abnormal skin color may be
important signs, capillary refill time becomes

h. 📖 ​Prevention
prolonged and this type of rash appears:
a. Exanthem subitum
b. Butterfly rash
● Patient education is key to the successful
management of HD. c. Purpura fulminans
● Patients should be: d. Forscheimer's spots
○ encouraged to ​be compliant with MDT​; e. Henoch-Schonlein purpura
○ educated about the signs and symptoms of
neuritis, and 6. Given to children 12 months and above as a single
○ advised to practice self examination and seek dose:
prompt medical care should they develop a. MC4-D
neuritis or other symptoms of clinical b. ACYW-135
exacerbations or leprosy reactions. c. MCV4-TT
○ Surgery and rehabilitation therapies as well as d. MCV4-CRM (IM)
counseling for the social and psychological
effects of the disease may also be required for
optimal outcomes. Answers: a,c,d,b,c,c
○ Patient reassurance of the ability to lead a
normal and productive social life and **********End of Transcription**********
education of the community, including refuting
myths and social stigma, are important parts of
management.

POST QUIZ

1. What is the hallmark clinical finding in Leprosy?

a. hypopigmented skin lesions with loss of
sensation
b. maculo-papular rash
c. Bull’s neck
d. petechiae

2. Characterized by the presence of single or multiple

skin lesions with a ​raised central area that would
appear like a mass.
a. Paucibacillary leprosy (PB)
b. Tuberculoid (TT) leprosy
c. Borderline Leprosy
d. Lepromatous Leprosy (LL)
3. The only bacterium known to infect Schwann cells
of peripheral nerves?
a. Mycobacterium tuberculosis
b. Mycobacterium bovis
c. Mycobacterium chelonae
d. Mycobacterium leprae

4. All of the following are true, EXCEPT?

7RANS FORMERS 8