GRAM-NEGATIVE BACTERIAL INFECTIONS

Patricia Austria-Cantimbuhan, MD
June 10, 2014; 8:00 10:00 AM
Pediatrics 2

OVERVIEW
Neisseria meningitidis
Neisseria gonorrhea
Hemophilus influenzae
Moraxella catarrhalis
Bordetella pertussis
Salmonella typhi
Shigella
E.coli
Cholera
Campylobacter jejuni
Yersinia pestis
Aeromonas hydrophila
Plesiomonas shigelloides
Pseudomonas aeruginosa
Burkholderia cepacia
Francisella tularensis
Brucella melitensis
Legionella pneumophila
Bartonella henselae

Viral respiratory infections, exposure to tobacco smoke, marijuana use,

binge drinking, attendance in nightclubs and college students living in
dormitories are associated with increased rates of meningococcal
carriage or disease . . .due to alteration of the mucosal surface and
enhanced mucosal binding and/or decreased clearance of the organism
from the nasopharynx.

Pathogenesis:
encapsulated meningococci colonizes the respiratory tract
of susceptible persons, either they become invasive or
antibody develops

NEISSERIA MENINGITIDIS
(MENINGOCOCCUS)

they adhere to the nonciliated, columnar epithelial cells in

the nasopharynx via pili.

ETIOLOGY
an encapsulated, oxidase-positive aerobic
diplococcus
appears as gram-negative, kidney-shaped pairs
13 meningococcal capsular groups, of which five are
responsible for cases of human disease (A,B,C,W135 and Y)

binding induces endocytosis of the meningococci into the

epithelial cell and penetrates the epithelial barrier via
phagocytotic vacuoles

if the antibody is insufficient and invasion occurs,the

individual may become bacteremic

The organism lives as a commensal in the nasopharynx of humans and is

typically carried by 10% or more of the population at any one time.

EPIDEMIOLOGY:
most often occurs in children 2 years of age or
younger; peak incidence occurs in children < 1yo;
another peak occurs in adolescents/ young adults.
TRANSMISSION: occurs from person-to-person
through aerosol droplets from the respiratory tract
and requires close contact
The human nasopharynx is the only natural reservoir
of Neisseria meningitides.

highest rate of meningococcal disease is found in a

multicountry belt across the sub-Saharan Africa
meningitis belt (serogroup A).
LOCAL DATA: Outbreaks occur in communities and
institutions, including child care centers, colleges
and military recruit camps.
Patients with persistent complement deficiencies or
anatomic or functional asplenia are at increased risk
of invasive and recurrent menigococcal disease.
INCUBATION PERIOD: 1-10 days, usually < 4 days

#3 lead to replication of the organism and establishment of a

carrier state; development of disease depends on the virulence of
the organism, innate susceptibility of the host and the presence/
absence of serum antibodies.
The most impt virulence determinant is the presence of a capsular
polysaccharide, which enhances resistance of the organism to
killing by normal human serum and helps resist opsonophagocytic
killing.
The severity of meningococcal dse is related to circulating level of
endotoxin (LOS lipooligosaccharide) in the bloodstream.

Young children due to immature alternative and lectin

complement pathways and lack of acquired serum antibodies;
Adolescents due to increased exposure from social activities.
Outbreak of Menigococcemia in the Phils:1 Oct 2004 to 28 Jan
2005: 98 cases (Baguio City 74, Mt.Province 22, Ifugao 2)
Case fatality ratio 33% 11 cases laboratory-confirmed

in developed countries (US, Europe) incidence 0.353.0 cases per 100,000 population, while in
developing countries 10-25 cases per 100,000
population.
Transcriber/s: Marie Mae G. Pantolla
Formatting: Marie Mae G. Pantolla
Editor/s:Marie Mae G. Pantolla

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CLINICAL MANIFESTATIONS:
ACUTE MENINGOCOCCEMIA presents with
pharyngitis, fever, myalgias, weakness, vomiting,
diarrhea, with/ without headache, fine
maculopapular rash, cold hands/ feet and abnormal
skin color
ACUTE MENINGOCOCCEMIA disease progresses
rapidly over several hours from fever without other
signs to septic shock characterized by prominent
petecchiae and purpura (purpura fulminans),
hypotension, renal failure, myocardial failure and
coma
MENINGOCOCCAL MENINGITIS presents with
headache, photophobia, lethargy, vomiting, nuchal
rigidity and other signs of meningeal irritation.
CHRONIC MENINGOCOCCEMIA characterized by
fever, non-toxic appearance, arthralgias, headache
and a maculo-papular to pustular rash, aften with a
hemorrhagic component; occurs rarely; symptoms
are intermittent with a mean duration of illness of 68wks

Drug (alternative) Dosage/ Route

Chloramphenicol
50-100 mkd
Ciprofloxacin
18-30 mkd
Meropenem
60-120 mkd
* Optimal supportive care is essential.
COMPLICATIONS
focal skin infarctions/ dry gangrene, adrenal
hemorrhage, endolphthalmitis, arthritis,
endocarditis, pericarditis, myocarditis, pneumonia,
lung abscess, peritonitis, renal infarcts, avascular
necrosis of the epiphyses
Deafness (5-10%) is the most frequent neurologic
sequelae of menigitis; others cerebral thrombosis/
infarcts, ataxia, blindness, CN palsies, paresis,
obstructive hydrocephalus
Nonsuppurative complications: arthritis and
cutaneous vasculitis

MM - indistinguishable frm meningitis due to other bacteria;

seizures and focal neurologic signs occur less frequently;
CM BCS usually positive but cultures may be sterile; may resolve
spontaneously, but meningitis can develop in untreated cases.

DIAGNOSIS:
Definitive Dx is established by isolation of
N.meningitidis from blood, CSF or synovial fluid

also identified in Gram stain preparation: Gramnegative diplococci and/or culture of petecchial or
purpuric skin lesion
others: rapid latex agglutination tests in CSF and
PCR assays
Culture results are often negative if the patient has been treated with
antibiotics; isolation of the organism from the nasopharynx is not
diagnostic.

Surveillance Case Definitions for Invasive Meningococcal

Disease
Confirmed
A clinically compatible case and isolation of N.
meningitidis from a usually sterile site: blood,
CSF, synovial fluid, pleural fluid, pericardial
fluid, isolation from skin scraping of petechial or
purpuric lesions
Probable
A clinically compatible case with either a
positive result of antigen test or
immunohistochemistry of formalin-fixed tissue
or a positive PCR test of blood or CSF without a
positive sterile site culture.
Suspect
A clinically compatible case and gram-negative
diplococci in any sterile fluid such as CSF,
synovial fluid or scraping from a petecchial or
purpuric lesion; Clinical purpura fulminans
without a positive blood culture

TREATMENT
-lactam antibiotics drug of choice, 5-7 days
duration
DRUG
DOSAGE/ ROUTE
Pen G
250,000-300,000 U/kg/day
Ampicillin
200-400 mg/kg/day
Cefotaxime
200-300 mkd
Ceftriaxone
100 d

Transcriber/s: Marie Mae G. Pantolla

Formatting: Marie Mae G. Pantolla
Editor/s:Marie Mae G. Pantolla

Diffuse Adrenal hemorrhage Waterhouse-Friderichsen

syndrome
PROGNOSIS
10% mortality rate (US)
poor prognostic factors: hypothermia or extreme
hyperpyrexia, hypotension or shock, purpura
fulminans, seizures, leukopenia, thrombocytopenia
(DIC), acidosis, high levels of endotoxin and TNF-,
presence of petecchiae <12 hrs before admission,
absence of meningitis, low/ normal ESR

Most deaths occur within 48 hours

Screening for complement deficiency after resolution of the
acute infection should be performed in older children, adolescents
and adults with meningococcal infection and in young children with
recurrent infection or with first episode caused by strains with
unusual capsular groups (W-135 or X).

RECOMMENDED CHEMOPROPHYLAXIS REGIMENS

FOR HIGH-RISK CONTACTS AND PEOPLE WITH
INVASIVE MENINGOCOCCAL DISEASE
Age
Rifampin
< 1 mo
> 1 mo
Adults
Ceftriaxone
< 15 yo
> 15 yo
Ciprofloxacin *
Azithromycin

Dose

Duration

5mg/kg PO q12
10mg/kg PO q12
600 mg PO q12

2 days
2 days
2 days

125 mg IM
250 mg IM
20mg/ kg PO
10mg/ kg

Single dose
Single dose
Single dose
Single dose

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Not for pregnant; not routinely recommended for

<18yo
PREVENTION: close contacts of pxs with
meningococcal dse are at increased risk for infection.
Antibiotic prophylaxis is indicated for household,
daycare and nursery contacts and for anyone who has
contact with the patients oral secretions during 7
days before onset of illness (within 24 hrs). Droplet
precaution for 24 hrs after initiation of effective
therapy.
Ciprofloxacin *- usually for adult

PREVENTION/ VACCINATION
INDICATION: for individuals at high risk (asplenia,
complement deficiencies, HIV, travelers to or
residents of areas where meningococcal disase is
hyperendemic/ endemic or belonging to a defined
risk group during an outbreak)
Children aged 9 months and above at high risk for
invasive disease should receive a two- doses
primary series MCV4 given 2 months apart
revaccination with MCV4 is recommended 3 years
following completion of primary series for those at
high-risk, with continued boosters at 5-year
intervals after the initial booster dose
if MPSV4 or bivalent vaccine are used as the first
dose, a second dose using MCV4 should be given 2
months later
* MCV4 (A,C,W-135, Y) meningococcal
conjugate vaccine (IM)
tetravalent MPSV4 meningococcal
polysaccharide vaccine (SQ);
Others: Bivalent (A,C) IM/SQ

NEISSERIA GONORRHEAE

Non motile, aerobic, non spore forming, gram

negative, intracellular diplococcus with flattened
adjacent surfaces
Optimal growth 35-37C, alkaline pH and in
atmosphere of 3-5% carbon dioxide

EPIDEMIOLOGY
Infection occurs only in humans
TRANSMITTION: through intimate contact and
rarely contact with fomites
Infection in newborn generally acquired during
delivery
ACUTE INFECTION begins 2-5 days after birth
It is the most common STI found in sexually abused
children
PATHOGENESIS:
Infects primarily columnar epithelium
Mucosal invasion results in local inflammatory
response that produces purulent exudate consisting
of PMN, serum and desquamated epithelium
Gonococcal lipo-oligosacharide (endotoxin) exhibits
direct cytotoxicity, causing ciliastasis and sloughing
of ciliated epithelial cells
Gonococcus transverses the mucosal barrier, the
lipo-oligosaccharide binds bactericidal IgM antibody
and serum complement , causing acute
inflammatory response in the subepithelial space
TNF and other cytokines are thought to mediate the
cytotoxicity of gonococcal infections
Transcriber/s: Marie Mae G. Pantolla
Formatting: Marie Mae G. Pantolla
Editor/s:Marie Mae G. Pantolla

CLINICAL MANIFESTATIONS

Asymptomatic Gonorrhea
Pharyngeal gonococcal infection
Rectal carriage asymptomatic in 40-60%
UNCOMPLICATED GONORRHEA
GENITAL primary infection develops
Urethra in males, vulva and vagina in prepubertal females, cervix post pubertal females
IP 2-5 days in men; 5-10 days in females
URETHRITIS
Purulent discharge, dysuria without urgency or
frequency
Untreated cases resolves spontaneously in
several weeks
Complication epididymitis, penile edema,
lympangitis,prostatitis,seminal vesiculitis
VULVOVAGINITIS
Pre-pubertal females:
Purulent vaginal discharge with swollen
erythematous, tender, and excoriated
vulva; dysuria may occur
Post- pubertal females:
Purulent discharge, suprapubic pain,
dyuria, dyspareunia, intermittent bleeding
RECTAL GONNORHEA
Often assymptomatic
May cause proctitis with symptoms of anal
discharge, pruritus, bleeding,pain, tenesmus
and constipation
GONOCOCCAL OPHTHALMITIS in newborn
Maybe unilateral or bilateral
Occur 1-4 days after birth
Infection begins with mild inflammation and a
serosanguinous discharge
Within 24 hours the discharge become thick and
purulent, tense edema of the eyelids and
marked chemosis occur
If not treated promptly corneal ulceration,
rupture and blindness may follow
DISSEMINATED GONOCOCCAL INFECTION
Hemtogenous dissemination in 1-3% of gonococcal
infection
Women account for majority of cases
Common manifestation:
Acute onset of arthralgia and fever( most
common)
25% complain of skin lesions
Asymmetric arthralgia
Petechial or pustular acral skin lesions
Tenosynovitis
Suppurative arthritis
Rarely carditis, osteomyelitis, and osteomyelitis
Dermatologic lesions begin as painful, discrete, 1-20
mm pink or red macules that progress to
maculopapular, vesicular, bullous, pustular or
petecchial lesions
The typical necrotic pustule on an erythematous
base is distributed unevenly over the extremities,
including the palmar and plantar surfaces, usually
sparing the face and scalp
Usually 5-40 lesions; 20- 40% may contain goncocci
TENOSYNOVITIS dermatitis syndrome
More common

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Fever, chills, skin lesions, and polyarthralgias

predominantly involving the wrist, hands and
fingers
BCS (+) 30-40 %
Synovial fluid CS almost uniformly negative
SUPPURATIVE ARTHRITIS SYNDROME
Systemic signs and symptoms are less
prominent
Monarticular arthritis often involving the knee
Synovial fluid CS (+) in 45-55%
Blood CS (-)

Patients beyond the neonatal period should be

treated presumptively for Chlamydia trachomatis

TREATMENT FOR INFANT AND PEDIATRIC

INFECTIONS
Uncomplicated Ceftriaxone 50 mg/kg/ in single
infection
dose IM; maximum 125mg
Bacteremia or
Ceftriaxone 50mg/kg/24hr for a
arthritis
minimum of 7 days
>45 kgs 10-14 days
Meningitis
Ceftriaxone 50mg/kg/dose q12
hr 10-14 days
Ophthalmia
Ceftriaxone 50 mg/kg/ in single
neonatorum
dose IM; maximum 125mg
Cefotaxime 100mg/kg/day single
dose IM
Endocarditis
Ceftriaxone 50mg/kg/dose q12
hr 28 days
Neonatal
should be treated parentally for
sepsis
minimum of 7 days
Cefotaxime is recommended for
patient with hyperbilirubinemia

DIAGNOSIS
depends on isolation of organism
URETHRITIS : Presumptive diagnosis
presence of gram(-) intracellular diplococci
Evaluated for concurrent syphilis, hepatitis B,
HIV and C. trachomatis infection
TREATMENT
Due to increase prevalence of penicillin resistant N.
gonorrheae, ceftriaxone is recommended as initial
therapy for all ages

UNCOMPLICATED GONOCOCCAL INFECTION: Treatment of children beyond the newborn period and adolescents
DISEASE
Uncomplicated
vulvovaginitis, cervicitis,
urethritis, proctitis or
pharyngitis
DGI (arthritis- dermatitis
syndrome)

<40kgs
Ceftriaxone 125 mg IM Single Dose OR
Ceftriaxone 8mg/kg, orally SD PLUS
Erythromycin 50 mg/kg oral x 14 d OR
Azithromycin 2o mg/kg oral SD
Ceftriaxone 50mkd IV/IM OD x 7d PLUS
Erythromycin 50mkd oral x 14d

Meningitis or endocarditis

Ceftriaxone 50 mkd IV/IM q12 for

meningitis duration 10-14 days PLUS
Erythromycin 50mkd oral X14d

Conjunctivitis

Ceftriaxone 50 mg/kg IM SD

PID

TREATMENT FOR ADOLESCENT AND ADULT

INFECTION
Single dose of ceftriaxone 125 mg IM eradicates
pharyngeal and uncomplicated urogenital infections
Safe in pregnant women
Other alternatives
cefixime 400 mg PO as single dose
ciprofloxacin 500 mg as single dose
Ofloxacin 400 mg PO
* Regardless of regimen chosen, treatment should
be followed by regimen active against C.
trachomatis
Doxycycline 100 mg BID x 7 days or
Azithromycin 1 gm in single dose per orem
Erythromycin is recommended for pregnant
women 7-10 day course

Transcriber/s: Marie Mae G. Pantolla

Formatting: Marie Mae G. Pantolla
Editor/s:Marie Mae G. Pantolla

>40 kgs
Ceftriaxone 25o mg IM SD OR
Cefixime 400mg oral, SD PLUS
Azithromycin 1g oral, SD OR
Doxycycline 100 mg oral 2x a day for 7 days
Ceftriaaxone 1g IV/IM OD x 7 d PLUS
Azithromycin 1g oral SD OR
Doxycycline 100 mg oral 2x /day for 7d
Ceftriaxon 1-2 g IV q 12 for meningitis duration 10-14 d ,
for endocarditis duration 28 d PLUS
Azithromycin 1g orally SD OR
Doxycycline 100 mg oral 2x/d for 7d
Ceftriaxone 1g IM SD PLUS
Azithromycin 1 g orally, SD OR
Doxycycline 100mg orally 2x/d for 7 days

PARENTERAL REGIMEN A
Cefocetan OR cefoxitin + doxycycline

PARENTERAL B
Clindamycin + Gentamicin

AMBULATORY REGIMEN
Ceftriaxone OR cefoxitin OR ceftizoxime OR
cefotaxime + Doxycycline w/ without
metronidazole

TREATMENT FOR DGI

Ceftriaxone 1 gram/24 hr IV recommended as initial
therapy
Alternative regimen
cefotaxime 1 gm IV q8
ceftizoxime 1 g IV q8
Patient hould be examined for clinical sign of
meningitis and endocarditis
meningitis 1-2 g q12 10-14 days
endocarditis 1-2 gm IV q 12 28 days
Gonococcal conjunctivitis treated with ceftriaxone 1
gm IM single dose
Treatment maybe switch to oral regimen 24-48 hour
when clinical improvement is obvious
cefixime 400 mg BID
cefpodoxime 400 mg BID
Concurrent therapy for treatment of chlamydia is
important!

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PELVIC INFLAMMATORY DISEASE

Encompasses a spectrum of infectious diseases of
upper genital tract due to N. gonnorhea, C.
trachomatis and endogenous flora (streptococci,
anaerobes, gram(-) bacilli
Recommended regimen
Cefoxitin 2 g IV q6
Cefotetan 2 g q12 plus Doxycycline 100 mg
BID PO or q 12 hr IV
Therapy is continued for at least 48 hours after
patient shows improvement . Thereafter
doxycycline is given for total of 10-14 days
COMPLICATIONS
PID
Endometritis
Ectopic pregnancy
Perihepatitis
Chorioamnionitis
Septic abortion
PREVENTION
Education
Use of barrier contraceptive
Early identification and treatment
Gonococcal opthalmia neonatorum
2 drops 1% solution of silver nitrate into each
conjunctival sac shortly after birth
Erythromycin(0.5%)
Tetracycline ophthalmic ointment

HEMOPHILUS INFLUENZAE
ETIOLOGY
fastidious, gram-negative, pleomorphic
coccobacillus that requires factor X (hematin) and
factor V (phosphopyridine nucleotide) for growth
Surrounded by polysaccharide capsule; six
antigenetically and biochemically distinct types (a
through f); the most virulent serotype belong to
serotype b; nonencapsulated strains lack capsule
genes and are designated nontypable.
EPIDEMIOLOGY
Humans are the only natural host.
Major reservoir: upper respiratory tract of young
infants/ toddlers
MODE OF TRANSMISSION: person-to-person by
inhalation of respiratory droplets or by direct contact
with respiratory tract secretions
Peak age for invasive Hib infections: 6-18 months of
age while for Hib epiglottitis: 2-4 years of age
Factors that predispose to invasive disease: sickle
cell disease, asplenia , HIV, immunodeficiency
syndromes, malignant neoplasms
Pre-vaccine era (1988), Hib was a major cause of
serious disease in children >90% in children < 5yo

PATHOGENESIS
Adherence to respiratory epithelium and colonization of the
nasopharynx mediated by pilus and non-pilus adherence factors

Mechanism of entry is influenced by cytotoxic factors

Once in the bloodstream, Hib resist intravascular clearance

mechanism due to the presence of a polysaccharide capsule

the magnitude and duration of bacteremia influence the likelihood of

dissemination to other sites like the meninges and joints

CLINICAL MANIFESTATIONS:(HIB)
Pneumonia
Bacteremia
Meningitis
Epiglottitis
Septic arthritis
Cellulitis (head and neck)
Otitis media
Pericarditis
Less common: endocarditis,endophthalmitis,
peritonitis, osteomyelitis, gangrene
Nontypable strains cause infections of the
respiratory tract (otitis media, sinusitis, pneumonia,
conjunctivitis); less often, bacteremia, meningitis,
chorioamnionitis and neonatal septicemia

Hib meningitis poor prognostic factors: SIADH and focal neurologic

deficits; sequelae behavior problems, language disorders, delayed
development of language, impaired vision, mental retardation,
motor abnormalities, ataxia, seizures, HCP
Hib cellulitis: cheek and preseptal region of the eye most common
sites of involvement
Arthritis: commonly affects large joints such as knee, hip, ankle,
elbow uusally single joint involvement

DIAGNOSIS
Established by culture growth of Hemophilus
influenzae from CSF, blood, synovial fluid, pleural
fluid or pericardial fluid (chocolate agar or blood
agar plates)
Gram stain of an infected body fluid specimen can
facilitate presumptive diagnosis
Others: slide agglutination serotyping, genotyping
by PCR

BCS medium chocolate agar or on blood agar plates using the

staphylococcal streak
All H influ isolates associated with invasive infxn should be
serotyped. Accurate serotyping is essential to monitor progress
toward elimination of type b invasive dse.

TREATMENT
Empiric Tx for invasive
Cefotaxime or
disease
Ceftriaxone (100mkd)
Alternative empiric agent
Meropenem (60-120mkd)
May be substituted if the
Ampicillin (200mkd)
Hib isolate is susceptible.
Duration: 10 days or longer via IV route

Transcriber/s: Marie Mae G. Pantolla

Formatting: Marie Mae G. Pantolla
Editor/s:Marie Mae G. Pantolla

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Dexamethasone (0.6mkd given q6 for 2 days) may be

beneficial for Tx in patients with Hib meningitis to
diminish the risk of hearing loss, if given before or
concurrently with the 1st dose antibiotic
Epiglottitis is a medical emergency; an airway must
be established promptly via ET or tracheostomy.
Infected pleural or pericardial fluid should be
drained.
Empiric treatment of AOM (acute otitis media) in
children <2yo or children >2yo or older with severe
disease: Amoxicillin 80-90mkd (high dose); for betalactamase producing isolates, use amoxicillinclavulanate, oral cephalosporins or azithromycin

PREVENTION
Post-exposure prophylaxis: Rifampicin is
recommended in households with a person with
invasive Hib disease and at least 1 household
member who is <4yo and unimmunized or
incompletely immunized.
Dosage: given orally once a day for 4 days (20mkd);
adult dose 600mg; not recommended for pregnant
women
VACCINATION
Indication: Hib vaccine
given at a minimum 6 weeks of age, with a
minimum interval 4 weeks; primary series 3
doses; booster dose should be given at 12-15
months of age with an interval of 6 months
from the 3rd dose
One dose of Hib vaccine should be considered
for unimmunized children age 5 years or older
who have the following (predisposed to Hib
disease): asplenia or those who had
splenectomy, sickle cell disease, stem cell
transplant, immunoglobulin deficiency,
leukemia, HIV infection
Universal immunization w/ Hib vaccine is recommended for all infants

MORAXELLA CATARRHALIS
ETIOLOGY
Gram-negative aerobic diplococci
EPIDEMIOLOGY:

Part of normal flora of the upper respiratory tract

infection occurs in all age groups

Most common in infants and young children

TRANSMISSION
presumed to be direct contact with
contaminated respiratory tract secretions or
droplet spread
CLINICAL MANIFESTATIONS
Acute otitis media
Sinusitis
Respiratory tract infection
Rare manifestations:
bacteremia
meningitis
conjunctivitis
endocarditis
shunt- associated
ventriculitis
Transcriber/s: Marie Mae G. Pantolla
Formatting: Marie Mae G. Pantolla
Editor/s:Marie Mae G. Pantolla

UTI
DIAGNOSIS
Culture on blood and chocolate agar media after
incubation in air or with increased carbon dioxide
TREATMENT
Amoxicillin remains as an effective empiric
treatment
Beta- lactam/ beta lactamase combinations
(amoxicillin-clavulanate)
Extended spectrum oral cephalosporins
Macrolides: Azithromycin, Erythromycin,
Clarithromycin , Trimethoprim-sulfamethoxazole
most strains produce -lactamase

BORDETELLA PERTUSSIS

tiny, fastidious gram-negative coccobacilli that

colonize only ciliated epithelium

1670 Sydenham first used the term pertussis meaning

intense cough
ETIOLOGIC AGENTS
Bordetella pertussis (95%)
Bordetella parapertussis (less frequent)
ETIOLOGIC AGENTS OF PERTUSSIS-LIKE ILLNESS:
adenoviruses
Chlamydia trachomatis
Mycoplasma pneumoniae
Bordetella pertussis
ANTIGENIC & BIOLOGICALLY ACTIVE COMPONENTS

fimbriae (pili)

filamentous hemagglutinin (FHA)

Pertussis Toxin subunit A(enzymatically active) &

subunit B (binding portion): major virulence protein

Adenylate Cyclase Toxin

Lipo-oligosaccharide (LOS)

Tracheal Cytotoxin

Pertactin
EPIDEMIOLOGY
60 million cases/ year worldwide, resulting in
>500,000 deaths
pre-vaccination availability, pertussis was a leading
cause of death due to communicable disease among
children; afterwhich, availability of vaccine led to
>99% decline
presently, resurgence in pertussis incidence and
shifting of burden of illness to young infants,
adolescents and adults

Epidemic pertussis in the 1990s

Change in epidemiology due to waning immunity postimmunization, an aging cohort who received less effective
vaccine and increased awareness and diagnosis

highest risk: infants & young children;

pertussis in adults impt source of infection in
unimmunized or partially immunized children
TRANSMISSION: by droplets from a coughing
patient that reach the upper respiratory tract of a
susceptible person

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transmissibility is greatest early in the illness

during the catarrhal and early paroxysmal
st
phases (until 1 2 wks after onset of cough)
INCUBATION PERIOD: 6-21 days, usually 7-10 days

indirect spread patient can contaminate the environment with

respiratory secretions; the host-to-be has contact with the secretions and
inoculates his or her own respiratory tract by the hands

STAGES
1. Catarrhal
stage

2. Paroxysmal
stage

3.

Convalescent
stage

lasts 1-2 wks

mild URI symptoms; recovery
rates of organisms and positive
cultures are highest
4 - 6 weeks
paroxysms of coughing
(hallmark) followed by an
inspiratory whoop; post tussive vomiting/ gagging
several wks to months;
gradual decrease in cough and
other symptoms

1. congestion, rhinorrhea, LG fever, sneezing, lacrimation, conjunctival

suffusion
2. coughing marks the onset; begins as dry, intermittent, irritative hack
and evolves into paroxyms
3. Number, severity and duration diminishes. Infants <3mo old: cyanosis
and apnea . Adolescents and adults, no distinct stages; duration >21 days
Catarrhal and paroxysmal- most infectious

CLINICAL CASE DEFINITION

A case diagnosed as pertussis by a physician or
a person with a cough lasting at least two weeks with
at least one of the following symptoms
Paroxysms (i.e. fits) of coughing
Inspiratory whooping
Post-tussive vomiting (i.e. vomiting
immediately after coughing) without other
apparent cause
CRITERIA FOR LABORATORY CONFIRMATION
Isolation of Bordetella pertussis or
Detection of genomic sequences by means of the
polymerase chain reaction (PCR) or
Positive paired serology
Bordetella pertussis
CASE CLASSIFICATION
Clinically confirmed: A case that meets the clinical
case definition but is not laboratory-confirmed
Laboratory confirmed: A case that meets the clinical
case definition and is laboratory-confirmed
Bordetella pertussis
DIAGNOSIS:
(+) leukocytosis (15,000-100,000 cells/ mm3) with
lymphocytosis in a child w/ chronic cough is a strong
indication of pertussis
Gold standard: culture
DFA (direct flourescent antibody)- a rapid test, esp.
in patients who have received antibiotics, but is only
reliable in laboratories with continuous experience
PCR test nasopharyngeal specimens not widely
available
Serologic tests - detection of a variety of antibodies
to components of the organism in acute and
convalescent samples
Transcriber/s: Marie Mae G. Pantolla
Formatting: Marie Mae G. Pantolla
Editor/s:Marie Mae G. Pantolla

TREATMENT
Treatment of choice: Erythromycin estolate
Dose:
children: 50 mg/kg q 6h x 14days
Adults: 2g/d q 6h x 14 days
Alternative agent:
Cotrimoxazole
Newer macrolides: Azithromycin or
Clarithromycin
Chemoprophylaxis:
Erythromycin: 40-50mkd po in 4 div doses, max
2g/day
Given to household and close contacts
regardless of age or immunization status

Goals of Tx: limit number of paroxyms, observe severity of cough,

provide assistance when necessary, maximize nutrition, rest and
recovery without sequelae
Erythromycin: risk for Infantile Hypertrophic pyloric stenosis;
infants <1 mo, give azithromycin
Isolation: 5 days after initiation of macrolideTx

COMPLICATIONS
Adolescents and adults: syncope, sleep disturbance,
incontinence, rib fractures, pneumonia
Infants: pneumonia (22%), seizures (2%),
encephalopathy (<0.5%), hernia, subdural bleeding,
conjunctival bleeding, death
Duration of classic pertussis: 6-10 weeks
VACCINATION
Primary series 5 doses as DTwP/ DTaP/ DT
Dose 1-3 given at 2-4-6 months of age
4th dose 12-18 months of age
5th dose 4-6 years of age
Given at a minimum age of 6 weeks with a
minimum interval of 4 weeks
Primary series, same as tetanus and pertussis
DT if pertussis is contraindicated.
INDICATIONS:
4th dose may be given as early as 12
months of age provided there is a minimum
interval of 6 months from the 3rd dose
5th dose may not be given if the 4th dose
was given at age 4 years or older
Note: Interruption of the recommended
schedule or delay in administering
subsequent doses during the primary
immunization does not reduce immunity or
necessitate restarting the series.
Patients recovering from diphtheria infection
should be immunized because infection does
not confer immunity.
After exposure to a case of suspect or proven
diphtheria, asymptomatic previously
immunized persons should receive a booster
of an age-appropriate diphtheria-containing
vaccine if at least 5 years from last dose.

Tdap
INDICATIONS:
approved as a one-time only substitute for
the next scheduled Td booster in those
individuals who completed the primary
series
preferred age for Tdap: 11-12yo

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an interval of at least 5 years is

recommended between Tdap and Td
thereafter, tetanus booster (Td) every 10
years
< 5years interval can be used when d px has
increased risk of exposure to or complications
from pertussis

SALMONELLA TYPHI (TYPHOID FEVER)

Gram negative bacilli

st
Attack rates: < 5yrs old; peak during 1 months of
life
INCUBATION PERIOD
Gastroenteritis: 6-48 hrs
Enteric fever: 3-60 days (usually 7-14 days)
Currently there are >2460 Salmonella serotypes:
most that cause human dse are divided among Oantigen grps A-E; serotype Typhi is classified in
serogroup D
Salmonella enterica serovar Typhi (Salmonella typhi)
S. paratyphi A
S. hirschfeldii (S. paratyphi C )
S. schotmulleri (S. paratyphi B)

NOMENCLATURE FOR SALMONELLA ORGANISMS

COMPLETE NAME

CDC
DESIGNATION

S. enterica subsp enterica

serotype Typhi
S. enterica subsp enterica
serotype Typhimurium
S. enterica subsp enterica
serotype Newport
S. enterica subsp enterica
serotype Choleraesuis
S. enterica subsp arizona
serotype 18:Z4,Z23:S. enterica subsp
houtenae serotype
Choleraesuis

S ser. Typhi

COMMONLY
USED NAME
S. typhi

S ser
Typhimurium
S ser Newport

S.
Typhimurium
S. Newport

S ser.
Choleraesuis
S ser. 18:Z4,Z23:-

S.
Choleraesuis
Arizona
hinshawii
S. marina

S. Ser Marina

S. serotype Typhi: found only in humans

Infection: direct contact with an infected person or
w/ an item contaminated by a carrier
INFECTING DOSE: 105-109 organisms
INCUBATION PERIOD: Enteric fever: 3-60 days
(usually 7- 14 days)
Chronic carriers: 1% of patients continue to excrete
Salmonella org. for > 1 yr

CLINICAL MANIFESTATIONS

fever, malaise, anorexia,, myalgia , headache,

abdominal pain, tenderness (2-3 days) diarrhea
pea soup consistency constipation stepwise,
unremitting fever within 1 wk
nd
2 wk : sustained high fever, fatigue, anorexia,
cough, abdominal symptoms increase in severity
mental depression, delirium, stupor acutely ill,
disoriented, lethargic
If no complications : resolve within 2-4 weeks
P.E. bradycardia disproportionate to fever
hepatosplenomegaly, distended abdomen and
diffuse tenderness
th
th
ROSE SPOTS on 7 to 10 day x 2-3 days (lower
chest/abdomen)
Chest : rhonchi and rales
Transcriber/s: Marie Mae G. Pantolla
Formatting: Marie Mae G. Pantolla
Editor/s:Marie Mae G. Pantolla

COMPLICATIONS
Intestinal perforation (lower ileum)
Severe hemorrhage
Toxic encephalopathy
Meningitis
Toxic myocarditis
Acute cholecystitis
Septic arthritis /Osteomyelitis
Pneumonia
Endocarditis
DIC
DIAGNOSIS
CBC : leukopenia with lymphocytosis,
normochromic, normocytic anemia
Cultures
Blood: (40-60%) 1st week
Stool / Urine culture after the first week
BMA highest positivity
Duodenal string capsule culture
Serology
PCR
Widals test results unreliable
4 fold rise in antibody titer
1:160 non-endemic area
1:320 endemic areas
Enzyme Immunoassay (Typhidot) :

acute infection
re-infection
NOT Typhoid

IgM
(+)
(-)
(-)

IgG
(-)
(+)
(-)

Resistance rates of S. typhi isolates

2003
2004
Chloramphenicol
1%
0%
Ampicillin
0%
1%
TMP-SMX
0%
1%

2007
8%
62%
1%

TREATMENT
Chloramphenicol: 50-100 mg/k/d q6 hours x 14
days
Alternative drugs:
TMP-SMZ 8mg/k/D 2 doses X 14 days
Amoxicillin 100mg/k/D PO 3 doses x 14 days
Ampicillin 200 mg/k/D 4-6 doses x 14 days
Cefixime 15- 20 mkd for 7- 14 days
Azithromycin 8-10 mkd for 7 days
Suspected Resistant Strains :
Cefotaxime: 150 - 200 mg/k/d q 6 hours
Ceftriaxone: 100 mg/k/d OD x 5-7 days
Ciprofloxacin : 20-30 mg/k/D 2 doses x 7-10
days
Corticosteroid : severe cases ; toxemia, delirium,
obtundation, stupor/coma or shock
Dexamethasone 3mg/kg for the initial dose,
followed by 1 mg/kg q6 for 48 hr
Chronic carrier state: excrete organisms for 1 year
High dose Ampicillin or oral Amoxicillin x 6 weeks
Cholecystectomy : chronic gallbladder infection

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PREVENTION
Active immunization
Parenteral purified Vi capsular polysaccharide
vaccine (Typhim Vi) - for children >2yo; single
IM dose, with booster every 2yrs., protective
efficacy 70-80%
Orally administered live attenuated vaccine
(Vivotif Berna) (Ty21 a strain of S. typhi ) for
children 6 yrs and above; not given to the
immunocompromised; efficacy 67-82% for 5
years
Typhoid vaccine
Indication:
given IM
recommended for travellers to areas
where there is risk of exposure to
Salmonella typhi and for outbreak
situations
given as early as 2 yo with
revaccination every 2-3 years if with
continued exposure
Other Recommendations:
Persons with intimate exposure to a
documented S. typhi carrier, such as
occurs with continuing household
contact
Laboratory workers who have frequent
contact with S. typhi and people living
in areas with endemic typhoid
infection
Other measures
proper waste disposal
personal hygiene
hand washing
sanitary practices

CAMPYLOBACTER JEJUNI

predominant sx: diarrhea (visible or occult bld in the

stool), abdominal pain, malaise, fever
Mild disease resembles viral gastroenteritis
Severe infxn mimic acute inflammatory bowel
disease
Immunoreactive complications occur during
convalescence: GBS, reactive arthritis, Reiter
syndrome, erythema nodosum

TREATMENT

erythromycin, azithromycin, doxycycline or

quinolones
Global zoonoses and among the most common causes of human
intestinal infections: Campylobacter coli

YERSINIA

YERSINIA ENTEROCOLITICA most common

Yersinia species causing human disease; produces
abominal pain that can mimic appendicitis and
diarrhea
Tx: TMP-SMX, aminoglycosides, 3rd gen
cephalosporins, quinolones
YERSINIA PSEUDOTUBERCULOSIS associated
with mesenteric lymphadenitis that produces an
appendicitis-like syndrome
Tx for culture-confirmed bacteremia: TMPSMX, aminoglycosides, ampicillin, 3rd gen
cephalosporins, chloramphenicol

Transcriber/s: Marie Mae G. Pantolla

Formatting: Marie Mae G. Pantolla
Editor/s:Marie Mae G. Pantolla

YERSINIA PESTIS agent of plague

3 principal clinical forms:
Bubonic (80-90%) most common
Septicemic
Pneumonic least common but most
dangerous and lethal
Treatment: Streptomycin, Gentamicin
alternatives: doxycycline, ciprofloxacin,
chloramphenicol

AEROMONAS AND PLESIOMONAS

Pathogenic gram-negative bacilli that commonly

causes enteritis and less frequently cause skin and
soft tissue infections and septicemia
common in fresh and brackish water and colonize
plants and animals
A. hydrophila, A. veronii and A. caviae are
associated with human infections
P. shigelloides most commonly associated with
acute enteritis

PSEUDOMONAS AERUGINOSA

Classic opportunist
Compromised host defense mechanisms due to
trauma, neutropenia, mucositis,
immunosuppression or impaired mucociliary
transport
Risk factors: prolonged hospitalization, use of
broad-spectrum antibiotics, chemotherapy,
mechanical ventilation and urinary catheters

CLINICAL MANIFESTATIONS
Primary and secondary skin infections: Burns and
wound infection, folliculitis, decubitus ulcers, etc
ECTHYMA GANGRENOSUM classic skin lesion,
begin as pink macules and progress to hemorrhagic
nodules and ulcers with ecchymotic and gangrenous
centers with eschar formation

External Otitis
Malignant otitis externa
Chronic mastoiditis
Keratitis
Endophthalmitis
Osteomyelitis/ septic arthritis (Stenotrophomonas
maltophilia)
Endocarditis (Stenotrophomonas maltophilia)
Pneumonia (Burkholderia cepacia)
CNS infection
UTI
Intestinal tract infection
Sepsis

DIAGNOSIS
blood, CSF, urine or needle aspirate of the lung, or
from purulent material obtained by aspiration of
subcutaneous abscess or areas of cellulitis
> 100,000 colony forming units/ ml of fluid or gram
of tissue is suggestive of invasive infection
TREATMENT
Dual therapy: 1-2 bactericidal agents
Ceftazidime
Ticarcillin-clavulanate
Cefipime
Piperacillin-tazobactam
Ciprofloxacin
Aminoglycosides for synergistic effect

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PREVENTION
Effective hospital infection control program
Hand hygiene

FRANCISELLA TULARENSIS

Tularemia zoonotic infection; human disease is

incidental and usually results from contact with
blood-sucking insects or live or dead wild animals.

BARTONELLA HENSELAE

CLINICAL MANIFESTATIONS

Lymphadenopathy
Fever
Ulcer/ eschar/ papule
Pharyngitis
Myalgias/ arthralgias
Nausea/ vomiting
hepatosplenomegaly

CLINICAL SYNDROMES IN CHILDREN

ULCEROGLANDULAR cervical or posterior
auricular nodes most commonly involved due to tick
bites on the head and neck

Glandular
Pneumonia
Oropharyngeal
Oculoglandular
Typhoidal
Others: meningitis, pericarditis, hepatitis, peritonitis,
endocarditis, osteomyelitis

TREATMENT
Streptomycin or Gentamicin for 10 days
Alternative: ciprofloxacin, doxycycline
PREVENTION
avoid exposure

DIAGNOSIS
Indirect Immunoflourescent Assay (IFA), enzyme
immunoassay, PCR
Predominant manifestation: regional
lymphadenopathy
Fever, mild systemic sx
Skin papule at site of bacterial inoculation
lymphadenopathy in 1 to 2 wks
Affected node suppurate spontaneously
Parinaud oculoglandular syndrome
Others: encephalitis, aseptic meningitis, FUO,
neuroretinitis, osteolytic lesions, hepatitis,
granulomata in the liver and spleen, pneumonia,
thrombocytopenic purpura and erythema nodosum
disease is self limited
Resolves spontaneously in 2- 4mos
Antibiotics: hasten recovery for acutely or severely
ill px w/ systemic CSD; TMP-SMX, Rifampin,
azithromycin, ciprofloxacin, gentamicin

BRUCELLA

LEGIONELLA PNEUMOPHILA

Legionnaires disease (mild to severe pneumonia)

characterized by fever, cough, progressive
respirotory distress; chills, myalgia, GI, CNS and
renal manifestations
Pontiac fever milder febrile illness without
pneumonia that occurs in epidemics and
characterized by an abrupt onset and self-limited
influenza-like illness
acquired thru inhalation of aerosolized water
contaminated with Legionella pneumophila

TREATMENT:
AzithromycinIV is the drug of choice
Levofloxacin (or other fluoroquinolones) for the
immunocompromised;
alternatives: doxycycline and TMP-SMX

Transcriber/s: Marie Mae G. Pantolla

Formatting: Marie Mae G. Pantolla
Editor/s:Marie Mae G. Pantolla

Cat-Scratch disease
Reservoir for human disease: cats
Cat fleas (Ctenocephalides felis) transmit the
organism between cats
INCUBATION PERIOD
from scratch to appearance of 1 cutaneous
lesion 7-12 d
from appearance of 1 lesion to appearance of
lymphadenopathy: 5-50 days

Brucellosis - a zoonotic disease of wild and

domestic animals; transmissible to human by direct
or indirect exposure to aborted fetuses or tissues or
fluids of infected animals or consumption of
products of infected animals
Humans are accidental hosts; people at increased
risk include those in farming, ranching, veterinary
medicine; meat inspectors and laboratory personnel
B. abortus (cattle), B. melitensis (goat/ sheep), B.
suis (swine), B. canis (dog) are known to infect
humans.
Treatment: prolonged antimicrobial therapy is
important; combination therapy is recommended.

AGE AND
CONDITION

ANTIBIOTIC

DURATION

> 8 yo

Doxycycline + Rifampin

6 weeks

< 8yo

Alternative: Doxycyline +
Streptomycin or Gentamicin
TMP-SMX + Rifampin

4-8 wks

Meningitis,
osteomyelitis,
endocarditis

Doxycycline + Gentamicin +
Rifampin

4-6 months

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-ENDTRANSCRIPTION DETAILS
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Transcriber/s: Marie Mae G. Pantolla

Formatting: Marie Mae G. Pantolla
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