PEDIATRICS II

Dr. Perfecto Soriano

BACTERIAL INFECTIONS

STAPHYLOCOCCAL INFECTIONS  PEPTIDOGLYCAN: elicits IL-1 production;

Etiology. chemotactic; activates complement; endotoxin-like;
 gram (+); ubiquitous; singly or in pairs, short chains or opsonin production
clusters  SLIME LAYER (in capsule):
 RESISTANT to high salt conc.; heat; drying prevents OPSONOPHAGOCYTOSIS
 aerobic or facultative anaerobes
 S.epidermidis, haemolyticus, saprophyticus: coagulase Epidemiology.
(-)  NON-pathologic  S. AUREUS:
 S. saprophyticus: mannitol (+); NOVOBIOCIN resistant  neonates and most children harbour them in their:
 S. aureus: coagulase (+)  nasopharynx
 produces WHITE PIGMENT  fingernails
 mannitol and acid phosphatase (-)  clothing
 variable hemolysis on blood agar  skin
 cell wall: peptidoglycan TEICHOIC ACID (50%;  rarely anus/vagina
repeating subunits of N-Acetylglucosamine) and can contaminate any site on skin or mucous
PROTEIN A membrane; or other persons (interpersonal
 virulence: production of enzymes & toxins transfer; air or direct contact)
 4 EXOTOXINS:  infection may follow colonization
1) α- toxin  tissue necrosis; platelet  FACTORS PREDISPOSING INFECTION:
aggreg.; leukocyte injury 1) malnutrition
2) β-hemolysin RBC hemolysis; 2) viral infection (resp. tract): e.g. measles
sphingomyelin degradation 3) previous antibiotic therapy (S. aureus resistant)
3) δ-hemolysin disrupts membranes 4) wounds
(detergent-like action) 5) skin disease
4) leucocidin toxic to phagocytes 6) ventriculoatrial shunts
 EXFOLIATIVE TOXINS A & B produce 7) corticosteroids
scarlatiniform rash: 8) acidosis
a) localized: bullous impetigo 9) azotemia
b) generalized: staph scalded skin syndrome 10) IV or intrathecal catheterization
 ENTEROTOXINS A, B, C1, C2, D, E, F
 food poisoning: ingestion of preformed Pathogenesis
enterotoxins A & B
 if intact skin & mucous membrane are breached by
 ENTEROTOXIN F:
trauma or surgey  organism can gain access to
 “toxic shock syndrome toxin” (TSST – 1)
underlying tissues LOCAL ABSCESS LESION
 rltmenstruation
 Adhesion to mucosal cells by: TEICHOIC ACID
 induces IL-1 and other cytokines
 virulence: protein A; leucocidin; hemolysin
 ENTEROTOXIN B
 increased susceptibility:
 assoc. w/ nonmenstrual TSS
 complement deficiencies
 Job, Chediak-Higashi, lazy leucocyte &Wiskott-
 ENZYMES: Aldrich syndromes (defective chemotaxis)
1) coagulase (clumping factor 0; clots plasma by  chronic granulomatous disease (impaired
interacting w/ fibrinogen) intracellular bacterial killing)
2) catalase (inactivates H2O2; for intracellular  HIV infections
survival)  diabetic ketoacidosis
3) penicillinase or β-lactamase (inactivates
penicillin at cellular level)
4) hyaluronidase (spreading factor)
5) phosphodiesterase

 PROTEIN A: reacts w/ Fc part of IgG; fixes complement;

antiphagocytic
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CLINICAL MANIFESTATIONS 4) hypotension (below 5th percentile for children
Skin and tissue infection. <16y/o, or orthostatic drop in diastolic BP of
≥15mmHg w/ change from lying to sitting)
 impetigo; folliculitis (may extend to deep seated
5) involvement of 3 or more of the ff:
furuncles or carbuncles if >1 hair follicle involved);
a. GI
paronychia; small furuncles
b. muscular
 cellulitis
c. renal
 Staphylococcal scalded skin syndrome (SSSS)
d. hepatic
 RITTERS DISEASE (in neonates)
e. hematologic
 by phage group II S. aureus
f. CNS
 starts ABRUPTLY; perioral erythema &
sunburnlike, tender rash (spread over entire Food poisoning
body in 2-3d), then appearance of bullae   self-limited disease
partial or total DESQUAMATION  ingestion of HEAT-STABLE ENTEROTOXINS preformed
 NIKOLSKY SIGN: peeling due to gentle by staph contaminating foods
stroking of apparently healthy skin  severe vomiting and watery diarrhea (2-6hrs after
 intraepithelial splitting at STRATUM ingestion)
GRANULOSUM (Unlike toxic epidermal  fever is ABSENT or LOW GRADE
necrolysis(TEN): splitting at  supportive therapy: FLUID REPLACEMENT
DERMOEPEIDERMAL JNX)
OTHERS:
Respiratory tract STAPH ENTEROCOLITIS
 otitis media; sinusitis; parotitis; tonsillopharyngitis;  Overgrowth of normal bowel flora
tracheitis  commonly follows use of BROAD-SPECTRUM ORAL
 PNEUMONIA: ANTIBIOTICS and STARVATION MALNUTRITION (in
 primary: hematogenous neonates)
 secondary: d/t viral infection such as in measles TROPICAL PYOMYOSITIS
 S. AUREUSIS a leading cause of pneumonia in  Localized or multiple muscle abscess, assoc. w/
malnourished children elevated muscles enzymes but WITHOUT SEPSIS
 high fever  prodromal symptoms:
 abdominal distention  coryza
 tachypnea  pharyngitis
 dyspnea  diarrhea
 diffuse bronchopneumonia  prior trauma
 lobar disease
MENINGITIS
SEPSIS  related to HEAD TRAUMA and NEUROSURGICAL
 together w/ bacteremia: in both normal and PROCEDURES; AMNIOTOMY; PARAMENINGEAL FOCI
immunocompromised and PERICARDITIS
 ONSET: sudden
ENDOCARDITIS
 fever; tachycardia; chills
 major complication of sepsis
 usually localizes in
 lungs
OSTEOMYELITIS and SEPTIC ARTHRITIS
 heart  MC cause in children in S. aureus
 joints RENAL AND PERINEPHRIC ABSCESS
 bones
Diagnosis.
 kidneys
 isolation from:
 brain
 skin lesions
Toxic Shock Syndrome  abscess cavities
 potentially FATAL condition by TSST-1 producing  blood
strains of S. aureus and possibly by enterotoxin  CSF
 5 major diagnostic criteria:  others
1) fever (≥38.8°C)  gram stain  coagulase and mannitol reactions
 sensitivity testing to antibiotics
2) presence of diffuse, macular erythroderma
3) desquamation (1-2wks after onset usu. in  PHAGE TYPING: in epidemiologic investigations
palms and soles)  ELISA or HEMOLYSIS: for Teichoic acid; α toxin;
peptidoglycan antibodies
 FOOD poisoning: thru clinical and epidem. findings

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Differential / Diagnosis
 skin lesions d/t S. AUREUS and GROUP A BETA-
HEMOLYTIC STREP.: indistinguishable
 KLEBSIELLA and other gram (-) or anaerobes: w/
pneumatoceles; pneumothorax; lung abscess

Treatment
 ORAL ANTI-STAPH ANTIBIOTICS
 Dicloxacillin;
 Cloxacillin;
 Amoxicillin PLUS Clavulanic acid,
 Cephalexin,
 Erythromycin and
 Clindamycin
 PENICILLIN SHOULD NOT BE APPLIED TOPICALLY !

 SERIOUS OR INVASIVE INFECTIONS:

 Nafcillin or Oxacillin IV
 (200-400mg/kg/d in 6 divided doses)
 infections d/t PENICILLIN-SENSITIVE
STRAINS OF S. AUREUS:
 Penicillin G
 PENICILLIN-ALLERGIC PATIENTS:
 Vancomycin;
 Cephalosporins should be used to treat
bacteremia d/t MRSA
INFECTIONS D/T OTHER COAGULASE NEGATIVE
 CNS INFECTIONS:
 Oxacillin or Nafcillin IV; STAPH (CoNS)
 Vancomycin,  CONS: Part of microbial flora indigenous to humans
 Trimethoprim-sulfamethoxazole or  S. EPIDERMIDIS  bacteremia in neonate w/ or
 Imipinem (for penicillin-allergic Px) w/o central venous catheter, in Patient w/ malignancy
or Bone Marrow transplantation, neutropenia and GI
Prevention. colonization
 CAREFUL HANDWASHING WITH A DETERGENT BEFORE  LINE SEPSIS: (found at exit site & tunnel tract)
AND AFTER HANDLING PATIENTS  Leucocytosis
 RECURRENT STAPH FURUNCOLOSIS should be given  Thrombosis
 Dicloxacillin or  Tenderness
 Clindamycin and  Erythema
 Hexachlorophene washes
 S. SAPROPHYTICUS  symptomatic urinary
infections in sexually active adolescent girls
METHICILLIN-RESISTANT S. AUREUS  S. EPIDERMIDIS  can cause asymptomatic UTI in
 major nosocomial pathogen among:
catheterized patient
 preterm infants
 w/ surgical wounds or burns Diagnosis
 prolonged IV lines or catheterizations  BACTEREMIA:
 prolonged hospitalizations  when blood culture grows rapidly (w/in 24hrs)
 contact with other infected Patients  when 2 or more blood cultures are (+) w/
 DOC: same CONS
 Vancomycinalone or  when the peripheral venous culture has a
 in combi. w/ Aminoglycoside or Rifampin higher quantitative colony count than that
 SUSCEPTIBLE TO: drawn from a central venous catheter
 Trimethoprim-sulfam. and
 Ciprofloxacin
 NOT SUSCEPTIBLE TO:
 Cephalosporins;
 Imipinems

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Treatment
 PENICILLIN-RESISTANT:
 give semisynthetic anti-staph Penicillin
 S. EPIDERMIDIS INFECTION:
 Vancomycin
 FOREIGN BODIES should be removed
Prognosis
 poor prognosis in INFECTED PROSTHETIC or ORIGINAL
HEART VALVES; in MALIGNANCY & NEUTROPENIA
STREPTOCOCCAL INFECTIONS
Etiology
 gram (+), spherical; in pairs/chains
 most: facultative anaerobic; some obligate anaerobes
 catalase (-)
 classified accdng to their ability to hemolyze RBC:
1) beta hemolytic: complete hemolysis
2) alpha hemolytic: partial “green” on sheep
erythrocytes (viridans group)
3) gamma hemolytic: no hemolysis
 serogroups on the basis of CHO components w/in cell
wall:
o group A through H and K through V

 GROUP A BETA HEMOLYTIC: cell wall M antigens:
resist phagocytosis and is the MAJOR VIRULENCE
FACTOR
 RHEUMATOGENIC: serotypes 1,3,5,6,18,19,24
 PYODERMA and GLOMERULONEPHRITIS:
serotypes 49,55,57
 GROUPS C and G: PHARYNGITIS, nephritis;
 BUT NOT RHEUMATIC FEVER!
 PYOGENIC TOXINS: responsible for the rash of
hemolysis (beta strains)
 ASO; DNAse B; hyaluronidase, NADase and
streptokinase  rise in serum (2-6 wks after infection)
Epidemiology
 Group A streptococci colonize nasopharynx
 (15-20% of normal children)
 infants have lowest incidence: d/t transplacental
antibodies
 PHARYNGITIS in temperate countries
 SKIN DISEASE in warmer weather
 GROUP A BETA HEMOLYTIC STREPTOCOCCI:
 spread by droplet (mostly); contact
w/ skin lesions or thru food, milk,
water
Pathogenesis
 Strep attach themselves to respiratory epithelial cells
by SURFACE FIBRILS and cell wall LIPOTEICHOIC ACID
 FIBRILS: w/ anti-phagocytic epitopes of type-specific M
proteins, which together w/ capsular hyaluronic acid,
resist phagocytosis
trans by: Lourdes L. Lorenzo Medicine
 extracellular digestive enzymes interfere w/ local
thrombosis (STREPTOLYSINS); pus formation (DNAse)
and enhance connective tissue digestion
(hyaluronidase)
 suppurative complications follow:
 local inflammation
 (peritonsillar or retropharyngeal abscess)
 direct extension (otitis media; sinusitis)
 lymphatic spread (lymphadenitis)
 bacteremia (sepsis, osteomyelitis, pneumonia)
Table 14.3. STREPTOCOCCAL SEROGOUPS MOST FREQUENTLY
INVOLVED IN HUMAN DISEASE
Serogroup Usual Clinical Feature
A Pharyngitis, Tonsilities, Otitis media, Sinusitis,
Scarlet fever, Erysipelas, Cellulitis, Impetigo,
Pneumonia, Endometritis, Septicemia
B Chorioamnionitis, Puerperal sepsis, Neonatal
sepsis, Meningitis
C Upper Respiratory Tract infections
Genito-urinary tract infections, Wound infections,
D
Endocarditis
Upper Respiratory infection, Cellulitis, Septicemia,
G
Deep tissue infections
Clinical Manifestations
 RESPIRATORY TRACT INFECTIONS (RTI):
o in infants below 3 mos, upper RTI presents as
pharyngitis, common cold or as both
simultaneously
o may be assoc. w/ acute otitis media or
impetigo
 TONSILLOPHARYNGITIS
o Group A strep
o 5-11y/o
o sudden onset of fever and sore throat PLUS
headache, nausea, vomiting, malaise,
abdominal pain
o ABSENT: cough, rhinorrhea, coryza,
hoarseness
o moderate to severe erythema of pharynx,
tonsils with tonsillar hypertrophy and white
exudates, palatal petechiae, swelling and
tenderness of anterior cervical nodes
 SCARLET FEVER
o SIMILAR to tonsillopharyngitis PLUS
additional tongue and skin changes
o “STRAWBERRY TONGUE”
o RASH: fine, red, blanching, rough,
sandpaper-like feel
o Circumoral pallor
o Pastia’s lines (accentuation in body crease)
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  STREP TSS
o clinical signs of severity: Differential Diagnosis
 hypotension,  PHARYNGITIS by:
 renal impairment,  diphtheria,
 coagulopathy, or  EBV,
 thrombocytopenia,  mycoplasma,
 liver involvement,  toxoplasmosis,
 adult respiratory distress syndrome,  TB,
 generalized erythematous macular rash  N. gonorrhea,
(may desquamate), or  N. meningitides,
 soft tissue necrosis (necrotizing fasciitis,  A. haemolyticum,
myositis, gangrene)  Y. enterolitica and
 SKIN INFECTIONS  Agranulocytosis
o MC is superficial pyoderma (IMPETIGO);
o others: ectyhma, cellulitis
o cellulitis: painful, erythematous, indurated
infection of the skin and subcutaneous tissue
w/ lymphangitis and regional lymphadenitis
 ERYSIPELAS
o acute, well-demarcated infection of the skin
with lymphangitis.
o advancing margins of lesions: raised, red, firm
 BACTEREMIA
o Sepsis may progress rapidly w/
hypotension, DIC, peripheral. gangrene
o metastatic foci  meningitis, brain
abscess, osteomyelitis, septic arthritis,
peritonitis, endocarditis
 VULVOVAGINITIS
o frequently caused by Group A beta
hemolytic strep in PREPUBERTAL GIRLS
o serous or serosanguinous discharge, marked
erythema and irritation of the vulvar area
 STREP PYODERMA: indistinguishable clinically
PLUS discomfort in walking and in urination
from Staph skin infection
Diagnosis
Complications
 THROAT CULTURE: gold standard for pharyngitis
 EARLY (SUPPURATIVE): local, lymphatic,
 ASO Titer: rises to >166 Todd units which is modified hematogenous spread
or removed by early antibiotic therapy
 LATE:
o HIGH in Rheumatic fever;
o SLIGHTLY or NOT ELEVATED in
o ARF (5 wks after pharyngitis)
glomerulonephritis; o GN (follow either pharyngitis or pyoderma)
o VARIABLE in pyoderma
in Group C or G Treatment
 Pen G
 DNase & hyaluronidase: HIGH in patients w/  Strep Pharyngitis:
pyoderma or pharyngitis  Pen V or
 Anti-Dnase: BEST SEROLOGY FOR PYODERMA  Long-acting Benzathine Pen G for non-
 Streptozyme: 2-min. slide test which detects compliant Patient or those w/ vomiting or
Antibodies (w/in 7-10 days of infection) diarrhea
 Rapid Diagnostic Tests: direct extraction of Group  Patient ALLERGIC TO PENICILLIN:
A CHO antigen from organisms obtained by THROAT  Erythromycin estolate or
SWAB  Erythroethylsuccinate
 Nospecific test: leucocytosis, elevated sediment
rate, C reactive protein

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  FAMILIES W/ MULTIPLE EPISODES OF DOCUMENTED,
SYMPTOMATIC PHARYNGITIS: should be cultured
simultaneously; those w/ Grp A Strep: treated w/
 Benzathine Pen G) and
 Recultured after 4 wks
 
 TREATMENT FAILURE:
o more common in oral than IM
o poor compliance
o reinfection
o presence of β-lactamase producing oral flora
o tolerant strep
o carrier state
 High doses parenteral Penicillin
o 400,00 u/kg/day
 Strep TSS,
 Erysipelas,
 Deep soft tissue infections,
 Meningitis,
 Sepsis,
 Bacteremia,
 Complications of Pharyngitis
Prevention
 Oral Penicillin prophylaxis (Pen V 250mg 2x a day)
INFECTIONS d/t Other Strep
 Group B (S. agalactiae)
o leading cause of neonatal sepsis and
meningitis
 Early onset Disease: (1st days of life)
o assoc. w/ OBSTETRIC PATHOLOGY:
(Prematurity, PROM or chorioamnionitis)
o usually presented as respiratory distress
 Late onset Disease: (1wk to 3mos)
o as sepsis, meningitis, focal infection
 Pen G: DOC of non-group A strep
 EXCEPT Group D (enterococci) and some α-
hemolytic strains where AMPICILLIN is the
DOC
 STREP VIRIDANS: MC etiology of infective
endocarditis in children;
 treated w/ PENICILLIN and
AMINOGLYCOSIDE
PNEUMOCOCCAL INFECTIONS
Strep.pneumoniae (Pneumococcus)
 major cause of:
 lower Respiratory Tract Infection,
 Bacteremia,
 Meningitis (all age groups)
trans by: Lourdes L. Lorenzo Medicine
 “fastidious”
 “lancet-shaped” gram + diplococcus (sometimes in
chains) w/ thick polysaccharide capsule
 similar in morphology to other Strep. (esp. α hemolytic
strep: normal flora of oropharynx)
facultative anaerobe; reduced O2 and increased CO2
environment
 81 serotypes
 QUELLUNG REACTION:
o capsular swelling (after mixing bacteria w/
anti-serum)
 serotypes 6,14,18,19,23: most pathogenic
 Illness: quite severe (6-24mos)
 Risk factors:
o Splenectomy or Asplenia
o Sickle cell disease
o Nephrotic syndrome
o Immunosuppressive therapy
 Mode of Transmission: originates from
oropharynx or nasopharynx hematogenous route or
direct extension
 otitis media
 acute suppurative meningitis
 in LOWER RTIs: predisposing viral infection
 damages ciliated mucosal epithelium  passage of
organism to lung parenchyma
 in TARGET ORGANS (i.e. lungs): neutrophils and
macrophages would invade  acute inflammation
reaction  repair and resolution (dependent on
development of Antibodies thru alternative pathway of
complement activation)
 ROLE OF PHAGOCYTOSIS: sign of factor in bacterial
eradication
Clinical Manifestations
 PNEUMONIA: Most common
 PULMONARY COMPLICATIONS:
 Empyema,
 Pleural effusion,
 Emphysema
 BRONCHOPNEUMONIA:
 fever,
 cough,
 nasal discharge  worsening cough
productive of copious purulent and rusty-
colored mucus
 SEVERE CASES: chest pains and DOB
 LEUCOCYTOSIS
 Chest X-ray: diffuse or focal pattern w/ segmental or
LOBAL involvement of lungs
 CSF: cloudy or turbid fluid w/ pleocytosis (>1000cells/
mm3) , predominance of PMNs. high protein and low
sugar
Page 6 of 39
  DEATH: d/t Pathogenesis
 overwhelming sepsis;  nasopharynx  mucosal surface penetration 
 respiratory failure in severe pneumonia and bloodstream by leucocytes  various organs
 cerebral edema or  circulating serum Antibodies and specific
 increased ICP and secretory IgA: protect the host from disease.
 herniation in meningitis
 Antigenic shift in pilial expression: may enable
organism to EVADE host defenses and could explain
Diagnosis persistence of nasopharyngeal carriage despite
 isolation of organisms from body fluids; culture; gram presence of group specific antibody
stain  Transplacental antibodies: until 3 months
 Latex Agglutination Test (LAT)  RISK FACTORS:
 countercurrent immunoelectrophoresis (CIE) 1) overcrowding
Treatment 2) poor health and living conditions
 Pen G (IV) and Pen V (oral): DOC 3) influenza
 Ampicillin 4) absent serum bactericidal activity
 RESISTANCE: mediated thru decreased affinity of 5) asplenia
6) agammaglobulinemia
penicillin binding proteins
7) inherited properdin
 Vancomycin,
8) C5-C8 deficiency
 Cephalosporins (newer gen),
9) Systemic lupus
 Carbapanems,
10) circulatory C3 nephritic factor disorder
 Quinolone
11) presence of HLA B27 complex
 SUPPORTIVE THERAPY:
o adequate Oxygenation
Pathology
o Fluids and Electrolytes  ACUTE INFLAMMATORY RESPONSE
o Maintenance of Respiratory support  w/ release of IL and TNF as reaction to
o Diminution of ICP and cerebral edema endotoxins leading to
o Surgical intervention 1) complement activation
2) diffuse vasculitis
Prevention 3) DIC
 23-valent pneumococcal capsular polysaccharide  Bleeding into adrenals may occur in SEPTICEMIA and
vaccine BUT they are poorly immunogenic esp. for high SHOCK (Waterhouse-Friderichsen syndrome)
risk group (<2y/o)
 vaccines are unable to utilize the help of
T-cells to stimulate antibody production, Clinical Manifestations
maturation of antibody response or dev’t of  incubation period: 1-10 days
immunological memory  upper RTIs w/ or w/o bacteremia
 prophylactic antibiotics  bacteremia w/o sepsis
 Ampicillin, Sulfisoxazole, Penicillin  meningococcimic sepsis w/o meningitis
 antimicrobials  meningitis w/ or w/o sepsis,
 meningoencephalitis
MENINGOCOCCAL INFECTIONS  focal organ infections
NEISSERIA MENINGITIDES
 gram (+), “biscuit-shaped” diplococcus FOUND  ACUTE MENINGOCOCCEMIA
ONLY IN MAN  initially as “influenza-like” illness w/ fever,
 MOST: fastidious, malaise, chills, arthralgias, headache, GI
 GROWTH: facilitated by incubation on blood, complaints
chocolate, Mueller Hinton, or trypticase soy agar in 5-  petechial, purpuric, maculopapular lesions
10% CO2 may develop w/in hours w/ subsequential
 ferments GLUCOSE and MALTOSE w/o gas formation hypotension, DIC, oliguria, renal failure and
 CANNOT ferment sucrose or lactose !!! coma.
 13 serogroups by capsular polysaccharides – A, B, C, X,  fulminant meningococcemia may occur
Y, Z, 29 – E and W – 135 w/ shock and often w/ adrenal hemorrhage
 SEROGROUP B: encountered more in the Phils that’s unresponsive to treatment
 MOT: person to person: respiratory droplets  assoc. w/ Endocarditis, myocarditis,
 DISEASE: more frequently in children <5y/o; pericarditis
 peak attack rate occurs in 6-12mos

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  ACUTE MENINGITIS Complications
 “classic signs and symptoms”  ACUTE:
 low incidence of assoc. seizures or focal  inflammatory response
neuorologic signs  infection or hypoischemic organ injury leading
to hypotension, myocardial failure, shock
 PRIMARY PNEUMONIA:  LATE
 15% have pleural effusions, ad empyema
 deposition of sterile immune complexes in
 PRIMARY ARTHRITIS: usually mono articular and joints or pericardium
often involves the knee  growth failure and skeletal deformities secondary to
 conjunctivitis, endopthalmitis, vulvovaginitis, bone infarction
radiculitis  Vitreous collapse and transient hemiballismus

 CHRONIC MENINGOCOCCEMIA Treatment

 Unusual;
 low-grade fever,  Pen G (IV) 300,000 u/kg/24hrs every 4 hrs for 7 days
 w/ rash resembling gonococcal infection,  Cefotaxime or Ceftriaxone: alternatives
 purulent arthritis,  CHLORAMPHENICOL: Patient w/ anaphylactoid
 erythema nodosum, type of penicillin allergy
 subacute endocarditis  ACUTE MENINGOCOCCEMIA:
 mean duration: 6-8wks  hourly vital signs,
 physical S/Sx, urine output,
Diagnosis  pertinent laboratory and hemodynamic data, plus
 fever, petechiae, abnormal mental status  medications
 Definitive Dx:  SEPTIC SHOCK: give..
o (+) culture of blood,  Dopamine or
o CSF,  Dobutamine
o skin petechiae or other sites of infections  Infants and children >2mos: give
 if antibiotics were given before specimen collection,
antigen detection tests of the CSF, serum, urine w/
 Dexamethasone
group specific-antisera can allow rapid diagnosis/
 PCR: directly from clinical specimens Prevention:
 ANCILLARY DATA:  Rifampin (DOC)
 Leucocytosis  alternatives:
 Thrombocytopenia  Ceftriaxone 125mg for children; 250mg for
 increased ESR and CRP adult given once
 Protenuria  Ciprofloxacin 500mg every 12hours for 5
 Hematuria days in adolescents
 in DIC: increased prothrombin factors V
and VIII  Routine vaccination of children:
 CH50 screens  NOT recommended!
 should be considered in children >2 y/o w/
Differential Diagnosis functional or anatomic asplenia, terminal
 petechial or purpuric rash similar in: complement or PROPERDIN deficiencies
 Dengue hemorrhagic fever
 Septicemia d/t other gram + or – org.  Vaccination can be an adjunct to
 Measles chemoprophylaxis
 Leptospiroses  to control outbreaks of disease caused by
 Kawasaki disease serogroups represented in the vaccine and may be
 Henoch-Schonleinpurpura given to travelers to endemic countries
 Steven-Johnson syndrome
 Idiopathic thrombocytopenia

trans by: Lourdes L. Lorenzo Medicine Page 8 of 39

Prognosis Epidemiology
 POOR IN:  Gonococcal infections occur only in humans.
 extremes of age
 dev’t of hypotension or shock  High prevalence among commercial sex workers (PH)
 respiratory, cardiac, renal failure  With higher prevalence among young adults between
 coma ages 15 and 24.
 rapidly progressive purpura - May be due to increasing problem of child and
 DIC teen- age prostitution.
 thrombocytopenia
 leucopenia  Newborns with Opthalmia Neonatorum
 low CSF PMN cell count - 1/3 of cases d/t gonorrhea
 high serum antigen conc. cell count - 1/3 to Chlamydia
 high serum antigen conc.
 low sedimentation rate  Patients with gonococcal infections commonly suffers
from other STDs such as Chlamydia, syphilis and
GONOCOCCAL INFECTIONS herpes.
 Reinfections are common esp. among sexually active
 Most Common cause of STDs
and promiscuous patients.
 most commonly involved: adolescents and young
adults  SOURCE OF ORGANISM: Exudate and Secretions
of infected mucous surfaces.
NEISSERIA GONORRHEAE
 gram (-) diplococcus; flattened sides  N. gonorrhea is communicable as long as an
 grows well in chocolate agar medium enhanced by individual harbors the organism.
presence of CO2  MODE OF TRANSMISSION:
 requirement for FREE IRON; relative sensitivity to cold
- Sexual intercourse
 Thayer-Martin medium: combines the use of - Oral-genital contact
antibiotics to inhibit growth of normal flora and
( organism isolated from pharynx, conjunctiva
nonpathogenic bacteria
and mucous membranes of sexual partner)
 useful in HIGHLY CONTAMINATED specimens
(pharynx, GIT, vaginal areas) - Fomites particularly in a crowded and
unhygienic environment ( rare)
 Plain Chocolate agar: in NORMALLY STERILE - Vertical transmission:
BODY FLUIDS (blood, urine, CSF, synovial) o Abortion in 2-35%
o Premature delivery in 17- 67%
 DIFFERENTIATION BETWEEN SPECIES: o PROM in 21- 75%
1) Sugar fermentation characteristics o Perinatal death in 2- 11%
2) presence of anti-genetically heterologous
o Normal term infants in 35- 77%
gonococcal pili
3) serum bactericidal activity
4) auxotyping w/c is based on the presence or  INCUBATION PERIOD: 2- 7 Days
absence of certain substances when the
organism is grown on various media
o ASYMPTOMATIC PATIENTS
5) antigenic characteristics of its so called  More likely to transmit infections since
PROTEIN I PROTEASE symptomatic patients usually cease
6) presence of monoclonal antibodies to the sexual activity and seek therapy.
protein I molecule
 More pathogenic: presence of pili in outer membrane
 VIRULENCE FACTORS:
1) pili
2) opacity proteins
3) ability to utilize iron
4) IgA protease
5) lipo-ologosaccharide
6) cell wall peptidoglycan

trans by: Lourdes L. Lorenzo Medicine Page 9 of 39

Clinical Manifestations  Some with observe staining of the
o Infection in children occur in three distinct age underwear
groups.  In many cases, patients might be
asymptomatic.
 DDx: T. vaginalis, diptheroids, pinworms,
 NEWBORN
Streptococci and Chlamydia
o NEONATAL OPTHALMIA
 Gonococcal opthalmia neonatorum o RARE MANIFESTATIONS
 Characterized by:  Pelvic Inflammatory Disease (PID)
 Rapidly developing thick  Perihepatitis
mucopurulent eye discharge  Urethritis
 Usually bilateral  Anorectal Infections
 Eyelid and conjunctival edema.  Tonsillopharyngeal infections
 SEVERE CASES: may be followed by corneal
ulceration and spread to other neighboring  ADOLESCENTS
tissues.  FEMALES
 Blindness results if left untreated.  Genital tract involvement in females is
 Some cases may be mild and self- limited. frequently asymptomatic
 Should always be differentiated from other  Manifests as:
causes of conjunctivitis.  Urethritis
 Endocervicitis
o NEWBORN ARTHRITIS  PID
 Commonly encountered during 2nd and 3rd  ECTOPIC PREGNANCY
week of life  May be considered since patient may
 Manifested by: present with acute abdomen and
 Fever fever, lower abdominal pain and
 Irritability with associated pain adnexal tenderness.
 Tenderness and limitation of  ASYMPTOMATIC INFECTION
movement in the involved joints.  Can lead to PID with tubal scarring
 Skin lesions ( older children)  Can result in ectopic pregnancy or
infertility.
o SCALP ABSCESSES  MALES
 Observed after application of scalp electrodes  Usually symptomatic
 Primary site- Urethra
o VAGINITIS
o Infection involving other mucous
o DISSEMINATED DISEASE WITH BACTEREMIA,
membranes can produce:
MENINGITIS AND ENDOCARDITIS
 Conjunctivitis
 Pharyngitis
 PREPUBERTAL CHILDREN  Proctitis
 Gonococcal infection usually occurs in the
o ARTHRITIS- DERMATITIS SYNDROME
genitourinary tract.
 Characterized by
o VAGINITIS
 Maculopapular rash w/ petechiae
 Most common manifestation in females  Tenosynovitis
 Symptoms vary in severity  Migratory arthritis
 Mild itching to the presence of  Meningitis
watery, mucopurulent vaginal  Endocarditis
discharge with dysuria and burning  Possible manifestations after hematogenous
sensation. spread of the organism.

trans by: Lourdes L. Lorenzo Medicine Page 10 of 39

 Treatment
Diagnosis
 GRAM STAIN AND CULTURE
 Exudates and secretions from mucous membranes
of involved tissues
 Essential in the diagnosis of gonococcal infections.
 OPTHALMIA NEONATORUM
 Demonstration of intracellular gram negative
diplococcic from conjunctival exudates
 Other specimens
 Urine
 Urethral discharge
 Vaginal discharge
 Blood
 Peritoneal fluid
 Synovial fluid
 CSF
 PREPUBERTAL GIRLS
- Vaginal specimens are adequate for diagnosis
- Endocervical specimens are unnecessary.
 At least 2 confirmatory bacteriologic tests involving
different principles (e.g. biochemical, enzyme
substrate or serology) should be performed.
 Caution should also be observe in interpreting the
presence of N. gonorrhea from the pharynx of young
children.
 SUSPECTED SEXUAL ABUSE
- Genital, rectal and pharyngeal cultures should be
obtained prior to institution of antibiotics.
- False positive results can occur in non-culture
gonococcal tests ( include gram stain, DNA probes
or enzyme immunoassay tests on oropharyngeal,
rectal or genital tract specimens)
- Should undergo tests for other STDs ( Chlamydia
infection, syphilis, heap B, HIV infection)
 Marked leucocytosis with increased ESR and acute
phase reactants are associated with SYSTEMIC
DISEASE.
 ADNEXAL INVOLVEMENT
Prevention
- Adnexal mass may be appreciated on
ultrasonography
trans by: Lourdes L. Lorenzo Medicine
 INITIAL THERAPY
 Ceftriaxone - extended spectrum
Cephalosporin
 Non- disseminated cases
(e.g. Opthalmia Neonatorum)
 Ceftriaxone 25-50 mg/kg/day IV or IM SD;
 not to exceed 125 mg.
 Cefotaxime- alternative 100 mg/kg IV or IM
 Buffered Saline solutions
 Used to irrigate the affected eye/s until
discharge has cleared.
 Equally important is treatment for possible
concomitant Chlamydia infection (co-infections
are common)
 Disseminated infections
 Duration of therapy is 7 days
 Ceftriaxone 25- 50 mg/kg IV or IM OD
 Cefotaxime 50- 100 mg/kg IV or IM q 12 hours
 Suspected Meningitis - therapy is prolonged
to 10- 14 days.
 Uncomplicated gonococcal infections beyond
newborn period and for adolescents
 Ceftriaxone 50 mg/kg/day IV or IM
 Disseminated infection  7days
 Meningitis  14 days
 Endocarditis  28 days
 ALTERNATIVE THERAPY
 Spectinomycin with or without a macrolide
(Erythromycin or Azithromycin)
 Adolescents and adults with uncomplicated
gonorrhea who became asymptomatic after
treatment need not be cultured for test of cure.
 Infected children should have follow- up cultures to
ensure that treatment id effective.
 To prevent neonatal infection, all pregnant women
should have endocervical culture examination as
part of prenatal care.
 High risk for infection  2nd culture late in pregnancy
should be obtained.
 Prevention of Opthalmia Neonatorum
Page 11 of 39
  Instillation of prophylactic agent into the eyes
of all newborns as soon as possible after delivery
and definitely within one hour after birth.
 Tetracycline (1%) ophthalmic ointment
 Erythromycin ( 0.5%) ophthalmic ointment
 Silver nitrate (1%) aqueous solution
 Case finding and reporting of children exposed to
sexual abuse prostitution is mandatory.
HEMOPHILUS INFLUENZAE
INFECTIONS
 Most common bacterial infection occurring in infants
and young children between 2 months and 3 years.
 Usual clinical presentations in children:
 Otitis media
 Acute bacterial meningitis
 Cellulitis
 Epiglotitis
 Pneumonia
Etiology
 MODE OF TRANSMISSION
 Direct contact
 Inhalation of droplets of secretions containing
the organisms.
Pathogenesis
 Upper respiratory tract  site of colonization
 Bacteria adhere to epithelial cells
 Viral infections such as influenza and respiratory
syncitial virus may promote acquisition and
colonization by H. influenza type b.
 Invasion of ciliated respiratory epithelial cells follows
with destruction of the infected cells.
 Production of polymorphonuclears (PMN) and
macrophages in the submucosa by inflammatory
response.
 Bacteria multiply rapidly in the blood
 BACTEREMIA PHASE
 Every serous compartment of the body may be
invaded.

 HEMOPHILUS INFLUENZAE
 Small pleomorphic gram-negative coccobacilli
Clinical Manifestations
appearance. o ACUTE BACTERIAL MENINGITIS
 Classified into the capsular serotypable strain:  Symptoms may be sudden or insidious
(types a to f)- the more invasive type, and the  Infants presents with:
 Irritability or incessant crying
non-encapsulated, non typable strain which can
 Progressive lethargy and stupor
also cause disease esp. in neonates and very
young infants.  Early Manifestations
 Fever
 Vomiting
 HEMOPHILUS INFLUENZAE TYPE B
 Poor suck
 Considered to be the most pathogenic and
 Late manifestations
invasive
 Seizures
 Cause majority (60-70%) of acute bacterial  Coma
meningitis in children below 2 years old.  Fulminant course may occur with rapid
 8- 12 % of type B: with β- lactamase production deterioration of sensorium, increasing ICP and
rendering them AMPICILLIN- RESISTANT. respiratory arrest within 24 hours after clinical
onset.
Epidemiology  RISK FACTORS FOR INCREASED MORBIDITY &
 Disease of very young infants MORTALITY
 Seizures
 Slight preponderance of:
 Coma
 male over females,
 Hypothermia
 non- whites over whites,
 Shock
 low over high socioeconomic groups and
 Age less than 2 months
 low birth weights.
 Hemoglobin <11gms/dl
 Increased risk of invasive disease is also shown in
 Pretreatment symptoms more than 3
immunocompromised patients.
days
 INCUBATION PERIOD: Less than 10 days
 CSF WBC < 1000/cu.mm

trans by: Lourdes L. Lorenzo Medicine Page 12 of 39

  Survivors may suffer from long term neurologic O EPIDIDYMITIS
sequelae that can cause significant handicaps in O UTI
later life. O BACTEREMIA
O ABSCESS FORMATION
o PNEUMONIA O NEONATAL SEPSIS
 Often preceded by cough and fever and other
Diagnosis
symptoms of URTI.
 Isolation of organism from infected body fluids
 AUSCULTATORY FINDINGS
 CSF
 May be minimal
 Urine
 May show crepitant rales or
 Blood
diminished breath sounds  Respiratory secretions
 SEVERE CASES  Pleural fluid
 Respiratory distress  GRAM- STAIN
 Dehydration
 Aid in initial therapy esp. in meningitis
 Metabolic imbalances
 IMMUNOFLUORESCENCE
 WBC elevated to about 15,000/ cu.mm
 Radiologic findings - vary from segmental or lobar  With use of acridine stain
involvement, single or multiple, with or without  Used for partially treated patients with
pleural reaction and pleural effusion. reduction of organism’s number in Gram
 With greater incidence and persistence of stain smears.
pleural reaction than from pneumonia  AGGLUTINATION TESTS AND
caused by Strep pneumonia. COUNTERCURRENT ELECTROPHORESIS
 Helpful in patients previously treated with
o OTHER MANIFESTATIONS antibiotics.
 Majority of Otitis media and sinusitis in  CSF IN MENINGITIS
children  Increase polymorphonuclear count
 Physical exam should include exam of middle ear >1000/mm3
and tympanic membrane for mobility in febrile  Increased protein level
infants without any obvious focus of infection.  Decrease sugar
 Older children (>3 years)  Finding usually persist despite 2 days of antibiotic
 More prone to development of Epiglottitis. therapy.
 Precipitous onset of fever and toxicity Treatment
 Dysphagia and drooling
 AMPICILLIN
 Usually assume a position of maximal
 DOC for initial therapy.
airway breathing
 Appears toxic- looking.  Ampicillin – resistant strains
 May be revealed by by lateral x-ray of the  ACUTE BACTERIAL MENINGITIS
neck.
 AMPICILLIN 200 mg/kg/ day +
CHLORAMPHENICOL 100 mg/kg/day both
o SEPTIC ARTHRITIS
in 4 divided doses.
 H. influenza as the 2nd most common cause.  AMPICILLIN can be used alone if organism
 Common in very young children shows sensitivity to it.
 Hips and shoulders are usually involved.  Duration of therapy
 10 days
O OSTEOMYELITIS
 Uncomplicated: 7 days
O ORBITAL CELLULITIS
O PERICARDITIS  Persistent / prolonged fever; with developing
O PERITONITIS complications  > 14 days

trans by: Lourdes L. Lorenzo Medicine Page 13 of 39

 Epidemiology
 2nd & 3rd GEN. CEPHALOSPORIN
 Alternative therapy
 CEFACLOR  otitis media
 CEFUROXIME & CEFTRIAXONE  attain
good antibiotic levels in CSF
 Meningitis
 Orbital cellulitis
 Septic arthritis
Prevention
 Capsular Polysaccharide (CPS) vaccine for H.
influenza
 Given starting at 2 months of age.
 HYPERIMMUNE GLOBULIN
 Prepared from adult donors immunized with
PRP vaccine.
 RIFAMPIN 20mg/ kg/ day for 4 days
Pathogenesis
 Prophylactic drugs for all contact personnel
 Eliminates 95 % of carriers
 Endemic throughout the world except in
developed countries
 Philippines
 cases are found throughout the year
 Higher prevalence occurring during cooler
months (December to Feb)
 Mainly disease of childhood: peak incidence 2-5
years
 Rare below 6 months – acquired immunity
 Mode of Transmission:
1. Through discharges and secretions from
lesions by direct or indirect contact with
patients or carriers
2. Through articles
 Can occur in immunized individuals
 PSEUDOMEMBRANE
- formed by leukocytes, fibrin, necrotic

DIPHTHERIA tissue and microorganisms, which is

adherent to the underlying tissues and leaves a
Etiology raw bleeding area when attached
 CORYNEBACTERIUM DIPHTHERIAE - Locations: nose, pharynx, larynx
 Slender, curved and slightly tapered clubbed - TOXIN
organism 1. contributes to further growth of lesion
 Gram- positive to variable, facultatively 2. elaboration of more toxins
aerobic 3. attacks myocardium, kidneys liver, cranial and
 Related to Mycobacteria peripheral nerves  foci of necrosis and
degeneration
 3 biotypes:
4. TOXIN is more absorbed on the upper than
1.) MITIS,
lower Respiratory tract.
2.) GRAVIS,
 Upper is more vascular
3.) INTERMEDIUS- related to severity of
infection
Clinical Manifestations
 ANTIGENS: K- Heat labile; O- heat stable
 INCUBATION PERIOD: 2 DAYS – 1 WEEK
 With 19 phage types
 Manufactures an EXOTOXIN  Features:
 Unstable; destroyed by light, heat and 1. Low-grade fever (<38C)

aging 2. TOXEMIA with rapid pulse disproportionate to

 Capable of damaging muscle esp. cardiac,
nerve kidney, liver and other tissues.
- AVIRULENT STRAINS  can become VIRULENT
after treatment with bacteriophage.
fever
 Classification is based on anatomical location
1. FAUCIAL
 Insidious onset with low grade fever,
malaise, headache, sore throat with slight
cervical lymphadenopathy

trans by: Lourdes L. Lorenzo Medicine Page 14 of 39

  Within 24 hours  pseudomembrane
appear as yellowish white spots on
reddened tonsils
 CLN enlarge further
 Prostration is prominent with rapid feeble
soft pulse and low BP
 Dysphagia and noisy brathing
 Nasal voice and and regurgitation of fluids
thorugh the nose due to palatal weakness
 “Bull neck appearance” due to
massive enlargement of LN
 DEATH: due to
 Bronchopneumonia
 Toxic myocarditis
2. LARYNGOTRACHEAL
 An extension of pharyngeal type
 More common in infants
 Hoarseness and barking cough
 Noisy breathing, followed by strider, aphonia
and marked dyspnea with supraclavicular and
suprasternal retraction
 SEVERE: prostration and progressive
obstruction  suffocation  cyanosis or
cardiac failure death
3. NASAL
 Occurs mostly during the first 3 years of life
 Tends to be benign
4. OTHER PARTS
 TOXIC PERIPHERAL NEURITIS
 May appear early or late
 May affect the palate, extraocular muscles,
diaphragm, skeletal muscles
 Gives rise to manifestations such as:
 Nasal regurgitation
 Strabismus
 Respiratory difficulty
 Limb or trunk weakness
 TOXIC NEPHRITIS
 With albuminuria, casts and edema
Diagnosis
 Early smears and cultures to identify the organism.
 Antitoxins and antibiotics are ALWAYS administered.
 SCHICK TEST
 Intradermal injection of dilute diphtheria toxin
 (+) reaction in patients without immunity,
hence susceptible to diphtheria.
 DIFFERENTIAL DIAGNOSIS
 NASAL DIPHTHERIA
o Presence of diphtheria membrane with
assoc. serosanguinous discharge.
o DDX
 foreign body
 nasal ulcerations
 ethmoiditis
 FAUCIAL DIPHTHERIA
o Diphtheric membrane is generally
darker, tougher and more adherent than
other pseudomembrane lesion.

 Conjunctivae O DDX
 Umbilical area of NB  Streptococcal and non-bacterial
tonsillopharyngitis
 External genitalia especially in FEMALE
 Infectious mononucleosis
 External auditory canal  Agranulocytic angina
 Wounds and ulcers in the skin  Leukemia
 Ulcers commonly on the legs  Herpetic infection
 Grayish membranes at the edges  LARYNGOTRACHEAL DIPHTHERIA
followed by atropic pigmented scarring. o Difficult to distinguish in the absence of
visible faucial or nasal membrane.
Complications
o Laryngoscopy may be necessary for
 BRONCHOPNEUMONIA & RESPIRATORY FAILURE
visualization and to obtain culture if a
 Common in the laryngeal type and in infants.
membrane is present.
 TOXIC MYOCARDITIS O DDX
 Produces cardiac manifestations
 Spasmodic croup
 Occur commonly during the FIRST 10- 14 DAYS.
 Acute laryngitis
 Acute heart failure may supervene anytime.
 Laryngotracheobronchitis
 Foreign body
 Retropharyngeal abscess

trans by: Lourdes L. Lorenzo Medicine Page 15 of 39


Prophylaxis
 DTP IMMUNIZATION
 Active immunity produced by the use of
toxoid.
 Protection for 10 years
 Booster doses given at suitable intervals until
childhood.
 Protection not absolute but disease becomes
milder with minimal complications.
 MOLONY TEST
 Indicates sensitivity to diphtheria toxoid
 Should be done in older children and adults
before toxoid is given to avoid severe reactions.
 PASSIVE IMMUNITY
 Administration of 10, 000 units of antitoxin
 Lasts for about 3 weeks.
Treatment
 DIPTHERIA ANTITOXIN
 Most important aspect of treatment
 Neutralize the toxin present in the general
circulation before it is absorbed by the tissues.
 Should be administered even before culture
results are available.
 Mild nasal or laryngeal cases
 40,000 u
 Moderately severe pharyngeal
 80,000 u
 Severe pharyngeal or laryngeal
 120, 000 u
 IV administration is preferred to neutralize
the toxin as rapidly as possible.
 For cases of sensitivity to horse serum:
 Fractional desensitizing doses are given
using Human Diphtheria immune globulin.
 Injections are given at 15 minute intervals if no
reactions are noticed.
 If there should be any reaction, one hour is
allowed to elapse and the last dose which did not
give a reaction is again given.
 EPINEPHRINE HCL (1:1000) SHOULD BE
READY IN CASES OF SENSITIVITY REACTION!!!
trans by: Lourdes L. Lorenzo Medicine
 PENICILLIN 100,000 u/kg/day IM/IV
 Given for 7 days to eliminate C. diphtheria in up
to 95% of cases
 Not a substitute for antitoxin!
Treatment of COMPLICATIONS
 CIRCULATORY COMPLICATIONS
 Anti-congestive failure measures
 Rest in fowler’s position
 Oxygen
 Digitalis
 Diuretics
 Low Na diet
 CORTICOSTEROIDS may be given
 Plasma or whole blood and vasopressors
are given as indicated.
 PARALYSIS
 treated by physical therapy
 High doses of Vitamin B may be tried
 RESPIRATORY DIFFICULTY
 Especially as found in laryngeal type
 High moisture atmosphere in a croup tent
 Performance of intubation or tracheostomy
as early as necessary for relief of dyspnea and
clearing of secretions from the airway.
Management of Contacts
 Contacts should be examined for Signs & symptoms
of early diphtheria
 Persons with (+) culture and who have not
received primary immunization should be treated
as a case of diphtheria
 If with (-) culture + immunized = given booster
shots
Management of Carriers
 Single course of treatment with PENICILLIN or
ERYTHROMYCIN.
 Repeat treatment if organism is not eradicated.
Page 16 of 39
PERTUSSIS (Whooping Cough)
 PERTUSSIS = “one hundred day cough”
 Common & serious infectious disease affecting the
respiratory tract of infants and children.
 Paroxysmal cough = bursts of short expiration ff.
by a long forceful inspiration producing distinct
sound called “whoop”
 Clinical presentation is most severe in infants and
children.
 Not all patients with pertussis whoop.
Etiology
 BORDETELLA PERTUSSIS
 Non- motile coccobacillary gram- negative aerobic
organism
 Oxidizes amino acids but does not ferment
carbohydrates.
 Multiplies and forms clusters on broncho-
epithelial cells of URT in infected persons.
 Grows easily in Bordet- Gengou agar.
 PHASE I- antigenic type
 Virulence is assoc.
 Strains responsible for transmission of
the disease
 Required for vaccine production
 Can be distinguished from B. parapertussis &
B. bronchoseptica by AGGLUTINATION
REACTION.
 MODE OF TRANSMISSION
 Contact with a patient
 Asymptomatic individuals rarely carry B.
pertussis.
Pathology
 Mucosal lining of respiratory tract is infiltrated with
lymphocytes and polymorphonuclear cells.
 Bronchial epithelium may show necrosis with
development of bronchopneumonia.
 Accumulation of mucous secretions- bronchiolar
obstruction and atelectasis
 Microscopic or gross cerebral hemorrhages may result
from brain anoxia.
 Encephalopathy and fatty infiltration of the liver have
been reported.
trans by: Lourdes L. Lorenzo Medicine
Clinical Manifestation
 Symptomatic illness starts within 1- 3 weeks
following inhalation of organism.
 TOTAL DURATION of illness varies from 6- 8 weeks;
may extend beyond 30 weeks.
 THREE STAGES
 INITIAL/ CATARRHAL STAGE
 Start as sneezing, runny nose, lacrimation, mild
cough
 Sometimes with low grade fever
 Often diagnosed as URTI
 Cough becomes more frequent after few days;
irritating especially at night.
 DURATION: 1-2 WEEKS
 MIDDLE/ PAROXYSMAL STAGE
 Coughing becomes more frequent and severe
towards end of 2nd week.
 1 expiratory phase = > 5 successive forceful
coughs
 After expiration, strong inspiratory effort is
exerted to inhale air through the small glottis
opening producing the “whoop”.
 May observe a protruding tongue, salivation,
bulging of eyes, lacrimation, distention of neck
veins, cyanosis.
 Episode repeated number of times before
successful clearance of airway by coughing out
tenacious secretion.
 Children vomit their food, sweat profusely, urinate
involuntarily and appear extremely exhausted and
lethargic.
 Epistaxis, periorbital edema, subconjunctival
hemorrhages and petechiae on face and neck may
be experienced.
 Convulsions caused by anoxia and intracerebral
hemorrhage.
 Child appears well and PE shows normal findings
in between episodes of paroxysmal coughs.
 Weight loss d/t poor appetite and vomiting.
 DURATION: 2- 4 WEEKS OR LONGER
 FINAL/ CONVALESCENT STAGE
 Less frequent & milder attacks of paroxysmal
cough
 Reduction of episodes of vomiting and seizures
 COMPLETE RECOVERY may be attained after 2- 3
weeks.
Page 17 of 39

Complications
 PNEUMONIA
 Most frequent complication
 Death usually among infants and children.
 Secondary bacterial infections are often the
etiologic agents.
 Forceful coughing may cause alveolar rupture
producing spontaneous pneumothorax and rarely
subarachnoid hemorrhage.
 Flare- up of latent tuberculosis infection may be
observed.
 OTITIS MEDIA
 Caused by S. pneumonia
 CONVULSIONS AND COMA
 May be due to cerebral anoxia or brain
damage following hemorrhages.
 OCCASIONAL COMPLICATIONS
 Rectal prolapsed
 Umbilical hernia
 Neurologic conditions (epilepsy, paralysis, visual
dysfunction, mental retardation)
Diagnosis
 WHO (1991) case definition of PERTUSSIS:
 > 21 days of paroxysmal cough + history of close
contact with a pertussis patient and either a (+)
culture of B. pertussis or a rise of antibody titer to
filamentous hemagglutination (FHA) or pertussis
toxin (PT) in paired sample
 CATARRHAL STAGE
 Diagnosis is not easy to establish
 End of catarrhal and during paroxysmal stage
 Marked leukocytosis
(20,000—50,000 cells/cumm) with absolute
increase in lymphocytes
 Radiologic findings (perihilar infiltrates, air
trapping, atelectasis) are not specific.
 Organism are best isolated during the early stage but
may be found on the epithelial surface of the
respiratory system throughout the disease.
 Not seen in other organs.
 Nasopharyngeal swabs may be cultured in
Bordet- Gengou medium.
trans by: Lourdes L. Lorenzo Medicine
Treatment
 ERYTHROMYCIN (50mg/kg/day) or AMPICILLIN
(100mg/kg/day)
 Shortens period of communicability but not the
duration of paroxysmal stage.
 Organism may be eliminated from epithelial
surface from 3- 5 days.
 DURATION OF THERAPY: 14 days
 Early administration during CATARRHAL STAGE
may abort pertussis.
 SUPPORTIVE THERAPY especially in infants with
PNEUMONIA
 Maintenance of fluids and nutrition
 Gentle aspiration of thick mucous
 Cough medications, anti-pertussis
gammaglobulin and steroids have not been
found effective.
Prognosis
 Death among infants due to bronchopneumonia and
other pulmonary complications.
Prevention
 Antibodies have been detected but there is no
evidence that can prevent the disease.
 IMMUNIZATION
 Active immunity by administration of WHOLE
CELL PERTUSSIS vaccine in combination with
DIPHTHERIA and TETANUS in 3 equal doses
given 4-8 weeks apart.
 Booster shot after a year and another booster
after 3- 5 years.
 ACELLULAR PERTUSSIS VACCINE
 Contains 2 major antigenic components of
B. pertussis
Prophylaxis
 EXPOSED CHILDREN <7 Y/O
 ERYTHROMYCIN for 14 days
 Active immunization for those who have not
completed their series of pertussis immunization.
Page 18 of 39
TETANUS
 An acute neurologic illness with severe muscular
spasms caused by Clostridium tetani in a
contaminated wound.
Etiology
 Clostridium tetani
 A motile, gram- positive, anaerobic rod
 Forms terminal spores resembling “drumsticks
or tennis racket”
 SPORES  resistant to boiling water and
disinfectants; destroyed by autoclaving.
 Survive in dry soil for years.
 VEGETATIVE FORMS  susceptible to heat,
disinfectants and antibiotics.
 Spores and vegetative forms are found in
intestinal contents in humans.
Epidemiology
 C. tetani spores are ubiquitous.
 Associated with contamination of umbilical stump,
chronic ear infections, puncture wounds in older
children, carious teeth, ear piercing, pregnancy
(postpartum removal of placenta and abortions)
 Not transmissible from person to person.
Pathogenesis
 Introduction of spore into damaged tissue
 Disease develops after conversion of spores to
vegetative forms which produce tetanospasmin
under anaerobic condition.
 TETANOSPASMIN
 Binds strongly to neural gangliosides
 Most important site of entry to NS is at the
alpha neuromuscular junction.
 Toxin travels retrograde toward CNS,
migrates trans synaptically and exerts the
most profound effect by inhibiting the spinal
presynaptic inhibitory synapses.
 Release of inhibition manifested as spasm of
agonist muscle groups.
 Antitoxin cannot neutralize the toxin once it
has been translocated into a neuron.
 Autonomic dysfunction can occur.
 C. tetani remains localized at the site of
injury with minimal tissue changes.
trans by: Lourdes L. Lorenzo Medicine
Clinical Manifestation
 INCUBATION PERIOD: 3-14 days after injury; may
range from 2 days-several months.
 5-14 days in neonates.
 Some will have no injury on site of infection
 Spores survive for months or years in a site of
previous injury and is activated by minor trauma
 In apparent site of infection from GIT or tonsillar
crypts.
 THREE CLINICAL FORMS
1. LOCALIZED TETANUS
 Pain and continuous rigidity and spasm of muscle
in areas contiguous to the wound.
 Lasts for weeks without sequelae or may
evolve into generalized tetanus.
2. GENERALIZED TETANUS
 Most common
 TRISMUS
 Early sign
 “Lock jaw”
 Associated with stiffness of the neck
muscles and difficulty in swallowing
 RISUS SARDONICUS
 “Sardonic grin”
 Due to spasm of facial muscles.
 OPISTHOTONUS
 Results from persistent spasm of the
back muscles.
 TETANIC SEIZURES
 Characterized by sudden burst of tonic
contraction of various muscles, with
flexion and adduction of the arms,
clenching of fists and extension of legs.
 Initially brief; later become prolonged and
exhausting.
 Precipitated by visual, auditory or tactile
stimuli.
 Consciousness is intact.
 Cyanosis and asphyxia result from spasm of
laryngeal and respiratory muscle.
 Dysuria and urinary retention may occur.
 fever usually mild but may be as high as 40 degrees.
 Disease lasts 2- 6 weeks.
Page 19 of 39
 3. CEPHALIC TETANUS
 Unusual form resulting from head wounds, chronic
otitis media or carious teeth.
 Dysfunction of one or more cranial nerves, most
often CN VII.
 Can remain localized or evolve into generalized
tetanus.
 NEONATAL TETANUS
 Generalized in type
 Starts as difficulty in sucking and irritability.
DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS
 Diagnosis is based on history and clinical presentation.
 History of absent or incomplete immunization and
history of trauma within previous 14 days is usual.
 History with the presence of trismus, generalized
stiffness, spasms and a clear sensorium are strong
evidences for tetanus.
 Lab studies are of little value.
 CSF is normal
 Elevated pressure
 EEG and EMG are non- specific.
 Minority will have positive gram stain or
wound culture (anaerobic)
 Recovery of organism does not prove dx of
tetanus since it can be part of the flora.
 Must be differentiated from other local & systemic
diseases that can simulate one or more of the clinical
findings.
 Trismus  observed in tooth and pharyngeal
abscesses, rabies and acute encephalitis.
 Bacterial meningitis  with nuchal rigidity.
 Tetany  carpopedal and laryngeal spasms.
 Strychnine poisoning may be clinically
indistinguishable except for the history and
biochemical Studies.
 Other conditions: dystonic drug reactions
(Phenothiazine) and epilepsy.
Complications
 SEPSIS & BACTERIAL PNEUMONIA
 Frequent causes of death in neonatal tetanus
 Malnutrition, dehydration, lacerations of the tongue
and vertebral fractures may develop.
trans by: Lourdes L. Lorenzo Medicine
 TACHYARRHYTHMIAS
 Widely variable blood pressure and unexplained fever
often occurs after few days of management of severe
generalized tetanus.
Treatment
 AIMS OF THERAPY
 Neutralize circulating toxin
 Remove the source of tetanospasmin
 Provide supportive care
 TETANUS IMMUNE GLOBULIN (TIG)
 500- 3000 Units IM, given immediately in a
single dose.
 TETANUS ANTITOXIN (TAT)
 SD of 20, 000- 50, 000 units can be given instead
of TIG.
 Half the dose IM and half IV after negative skin
test or after desensitization.
 Wounds should be cleaned and debrided
immediately, foreign bodies removed and wound
left open.
o Antitoxin and sedation should be given
prior to these procedures.
 Excision of umbilical stumps no longer
recommended!
 PENICILLIN G (100.000 U/KG/24 HOURS) IV
 DOC; In 6 divided doses for 10 days
 In ALLERGIC PATIENTS:
 Metronizadole or
 Tetracycline as effective alternative.
 Patient should be placed in a quiet, intensive care
setting with minimal auditory and visual stimuli.
 BENZODIAZEPINES
 Mainstay of therapy
 DIAZEPAM  used frequently; effective in
controlling hypertonicity and spasms.
 Used in initial dose of 0. 5 mg/kg IV push
and repeated after 2-4 hours for
recurrent seizures
 As maintenance IV drip of 20- 40 mg (NB)
or 20-80 mg (children).
 Dose is titrated to control spasms as
needed and tapered as spasms decrease.
 Therapy may be continued for 2- 6 weeks.
Page 20 of 39
  Barbiturates, Chlorpromazine, Mephesin, Chloral
hydrate and Magnesium sulfate have been used.
 Pyridoxine  added as treatment of tetanus.
 Coenzyme for the conversion of glutamic acid
to GABA (presynaptic inhibitor in the spinal
cord)
 COMBINATION THERAPY
 Diazepam (IV push & drip),
 Phenobarbital (10-15 mg/kg/day),
 TIG (500 units) or
 TAT (20,000 u) and
 Pyridoxine (100 mg/kg/day for 7 days)
any of the above + Penicillin G
 RESPIRATORY PARALYSIS:
 Pancuronium bromide / vecuronium
(0.1 mg/kg/hr continuous infusion)
 Endotracheal intubation
 Artificial ventilation
 Adequate fluid, electrolytes and calories should be
maintained.
 TACHYARRHYTHMIAS, Symptoms of
AUTONOMIC INSTABILITY
 Beta- adrenergic blocking agents
(PROPANOLOL)
 Combined beta & alpha adrenergic blockers
(LABETALOL)
 Magnesium sulfate
Prevention
 TETANUS TOXOID IMMUNIZATION
 Adsorbed toxoid preferred since immunity
lasts longer.
 Infants: 3 doses of DPT at 2 months interval
 Starts at 2 months of age
 4th dose of DTP or DTaP at 12 months after
the 3rd dose.
 5th dose at 4-6 years of age.
 TT booster should be given every 10 years.
 Unimmunized pregnant women
 2 doses of TT at least 4 weeks apart
 2nd dose given at least 2 weeks before
delivery.
 Children not immunized by 6 y/o
 Give 3 doses of adult type Td.
trans by: Lourdes L. Lorenzo Medicine
 Following INJURY
 Preventive measures are dictated by
immunization status and characteristics of injury.
 If with active immunization/ status is
UNKNOWN; wound is not minor or clean
 TIG (250-500 u) IM or
 TAT (3,000- 5,000 u) IM
*Skin testing is mandatory!
 Wounds contaminated with dirt, feces or saliva,
puncture and crush wounds, avulsions, frostbite
and missile wounds are tetanus prone.
 FOR ACTIVE IMMUNITY
 TT given at the same time as TIG or TAT in
another site and in a separate syringe.
 TT BOOSTER
 Given if child had at least 4 dTP
 Wound is not minor or clean
 5 or more years has passed since the
4th injection.
 If wound is clean and minor, 10 years can elapse
before TT is given.
Prognosis
 Highest mortality is found in extremes of life.
 Case fatality rates for neonatal tetanus is from
35-50 %
 Poor prognosis is associated with
 Short interval (< 7 days) between injury or birth
and trismus
 Short progression (<3 days) from trismus to
generalized spasms.
 Late administration of TIG or TAT,
 inadequate supportive care and
 presence of complications also adversely affect the
prognosis.
 Following up of survivors of neonatal tetanus showed
neurologic sequelae
 Spasticity
 Paralysis
 Seizures
 Mental deficit
 Behavioral problems
 Active immunization following recovery is imperative
because the quantity of tetanispasmin required to
produce tetanus in insufficient to induce a protective
immune response.
Page 21 of 39

SALMONELLOSIS
 Infection with salmonella organisms have became the
most widespread animal borne disease in the world.
Etiology
 3 MAJOR SALMONELLA SPECIES:
 S. typhi  1 serotype
 S. cholerasuis  1 serotype
 S. enteritidis  > 2,000 serotypes
 Other serotypes  non-typhoidal Salmonella
usually manifests as gastroenteritis or
enterocolitis; may produce bacteremia and
localized infections.
 S. typhi  causes typhoid fever
 Salmonella  grouped according to serogroups
 Group A, B, C, D and E
 Only the following have human as their natural
reservoir:
 S. typhi
 S. paratyphi A
 S. paratyphi B (S. schottmuelleri) and
 S. paratyphi C (S. hirschfeldii)
Epidemiology:
 Incidence is increasing particularly in countries
like the Philippines where there is lack of
adequate clean water supply and animal hygienic
and standards are not being followed.
 TRANSMISSION: via the fecal oral route via
contaminated water and food mainly meat and
poultry.
 Food handlers = are the main source of
infection but the presence of other animal
reservoirs such as chicken, cattle, pigs and turtles
leads to increased incidence of illness.
 VECTORS:
 Fomites
 Soap
 Baths
 Air filters
 Dyes
 Cosmetics
 Medical instruments
(thermometers, NGT)
 10% of Filipino children is due to Salmonella with all
age group susceptible but is more severe in the
newborns, young infants, and the elderly.
trans by: Lourdes L. Lorenzo Medicine
 Recent evidence shown Salmonella as significant cause
of pneumonitis,, meningitis, and children less
than 3 mos. old
 Patients with immuno-deficiency syndromes
particularly in HIV are highly susceptible to Salmonella
Pathology:
 Salmonella maybe found in the GIT of asymptomatic
individuals
 Development of infection and symptoms depends on a
variety of host and agent factors.
 HOST FACTORS:
 Acid pH of stomach
 Gastric emptying time
 Presence of normal GI flora
 Intachhumoral mechanism &
macrophages
 Number and virulence of organism contribute also
to the development and severity of the disease.
 Pathogenesis of NON-TYPHOIDAL SALMONELLA
involves:
 Mucosal inavasion of the ileum and
colon resulting in brush border damage.
 Release of substances such as
prostaglandin in addition to mucosal
damage contribute to the mechanism of
diarrhea.
 Unlike the shigella, ulcerative and
necrotic lesions are seldom seen.
 With S. typhi and S. paratyphi invasion
of the mucosa and lymphoid tissue occur
with the intra-phagocytic survival and
subsequent systemic spread.
 In the peripheral blood mononuclear
predominance is seen in typhoid in contrast
topolymorphonuclears in non-typhoidal
salmonellosis.
Clinical Manifestation:
1. GASTROENTERITIS
o MOST COMMON clinical entity caused by
salmonella particularly the non-typhoidal
varieties and is known as Salmonella food
poisoning
o Ingestion of the organism may cause diarrhea
after a few hours to a few days of incubation.
o Diarrhea is indistinguishable from those
caused by other etiologic agents with nausea,
vomiting, headache and abdominal cramps.
o Stools are characterized as mucoid to bloody
with accompanying increased flatulence.
Page 22 of 39

2. BACTEREMIA with or without localized
suppurative lesions.
o Invasion from the the GI tract occurs when
the host defenses are usually low resulting in
bacteremia which about 10% of cases results
in localization and development of
suppurative lesions
o ORGAN involvement: lungs, kidneys,
meninges, bone, endocardium, pericardium
and less commonly the femoral and distal
aorta, peritoneum, middle ear, genitals,
prostate and fallopian tube.
o Meningitis is more common in in newborns
while osteomyelitis is usually found in those
with underlying bone injuries.
o SYMPTOMATOLOGY includes; high grade
fever with chills and other signs referable to
the tissue or organ involved.
3. ENTERIC FEVER
o General term which refers to a characteristic
prolonged fever usually caused by a S. typhi
and is known as TYPHOID FEVER.
O It can also be caused by other non-typhoidal
Salmonella hence the name ENTERIC FEVER.
o Other organisms associated with
ENTERIC FEVER:
 S. paratyphi A and B,
 S. cholerasuis,
 S. typhimurium.
o Onset is insidious and fever maybe
accompanied by:
 headache,
 prostration malaise,
 anorexia, and
 myalgia with alternating
constipation and diarrhea.
o Other manifestation:
 Mental disorientation
 Confusion
 Hepatomegaly
 Splenomegaly
 Generalized lymphodenopathy
 Occasional bradycardia
 Respiratory symptoms more
common in children.
trans by: Lourdes L. Lorenzo Medicine
4. ASYMPTOMATIC ACUTE OR CHRONIC
CARRIER STATE
o Excretion of the organism in asymptomatic
individuals may be found in about 7-9% of
Filipino children less than five years old
o Acute carriers usually follow ingestion of the
organism as what occurs in newborns and
young infants while the chronic carriers
develop in about 1-4% of gastroenteritis and
or enteric fever cases.
o Elderly- chronic carriers are often associated
with BILIARY DIASEASE
o Asymptomatic state carrier state being quite
common contributes to difficulties in control
of the spread of organism.
Complications:
 Are due to the septic localization of the
organisms in the body which give rise to:
 Pneumonia
 Pyelonephritis
 Meningitis
 Osteomyelitis
 Arthritis
 Pericarditis
 Endocarditis other local lesions
 Severe dehydration and shock may occur.
 Hemorrhage and perforation are rare.
Diagnosis:
 Isolation of the organism from the blood, stool,
urine, spinal, fluid, bone marrow or pus from a
suppurative lesion, depending on the tissues
involved.
 The bone marrow has been proven to be a
reliable source for culturing the organism
especially because bacteremia is intermittent and
decreases rapidly after the first week of illness.
 OTHER TESTS:
 Serologic titers using passive
hemagglutintation assay (PHA),
 Latex particle agglutination slide test
 Counter immunoelectrophroses (CIE),
 ELISA and fluorescent antibody test (IFA).
 The more recent ones are DNA probes,
 Phage typing and
 Chromosomal analysis.
Page 23 of 39
Treatment:
Gastroenteritis and the carrier state
 No specific antimicrobial therapy is
recommended unless…
1.) the patient is below 3 months,
2.) has an underlying immunocompromised
condition or
3.) is highly susceptible to invasive disease.
 Antibiotics have not been proven to effectively
eradicate the organism from the stools and may
even prolong the carrier state.
 Acute diarrheal disease
 necessitates correction of dehydration and
electrolyte imbalance,
 treatment of shock,
 proper management of nutrition and
 institution of measures to prevent further
diarrhea.
 For Enteric fever and Septicemia, with or
without localized infections, empiric therapy
remains to be:
 Amoxicillin/Ampicillin,
 Chloramphenicol or Cotrimoxazole.
Prevention:
 Good sanitation
 Thorough cooking of food stuffs derived from
potentially contaminated sources
 Proper storage of food
 Prompt recognition and control of infection
among domestic animals
 Proper meat and poultry inspections
 Food handlers, inhabitants of towns along
lakes, rivers and seacoasts, residents in
localities with inadequate toilet facilities,
health workers, and travelers should be
vaccinated.
 Vaccination againts typhoid confers certain
degree of protection which may last up to
two to three years, but hygienic measures
should be stressed.
Prognosis:
 Depends on the clinical type and severity of the
infection.
 The prognosis in the septicemic form is poor.
 Severe gastroenteritis particularly in the
undernourished infants maybe fatal if prompt
treatment is not instituted  development of
meningitis
trans by: Lourdes L. Lorenzo Medicine
TYPHOID FEVER
 A general infection cause by Salmonella typhi
involving primarily the LYMPHOID TISSUES (Peyer’s
patches) of the small intestine.
 The clinical manifestation varies considerably from one
case to another and these generally depend upon the
age of the individual, the rapidity of the onset and
persistence of the BACTEREMIA.
Etiology and Epidemology:
 Caused by Salmonella typhi, a gram-negative
motile and non-spore-forming bacillus.
 The infection is frequently contracted from
contaminated food like milk, milk products, sea
food and shellfish, and by drinking contaminated
water.
 Flies may be a vector in the transmission of
typhoid fever. Asymptomatic carriers, especially
food handlers, are responsible for infecting a
large number of cases.
 Has a world-wide distribution, and is endemic
particularly in areas of low sanitation levels like
urban deprived communities.
 It occurs any time of the year but especially from
May to August.
 The infection is most commonly seen in
individuals between 16 and 30 years of age, but
all ages may be affected including the very young.
Pathogenesis:
 Invasion of the blood stream occurs through the
upper intestinal tract and the organisms localize
in the reticuloendothelial system, with
hyperplasia and hypertrophy of the lymph nodes
and follicles and enlargement of the spleen and
liver.
 The bacteria then reinvade the blood from these
foci and multiply in different organs, particularly
the gall bladder from where they are discharge
into the intestines. They then penetrate the
lymphoid tissue of the small intestine and
proximal colon, especially the Peyer’s patches,
and there are areas of focal necrosis and
ulceration.
 A prominent microscopic finding is
erythrophagocytosis and scattered infiltrates of
lymphocytes and plasma cells in and about these
foci.
 Characteristically, there is absence of
polymorphonuclear leukocytes.
 Hemorrhage and perforation due to extension of
the lesions may occur.
Page 24 of 39
Clinical Manifestations:
FETAL TYPHOID
 The fetus maybe infected if a pregnant woman
contracts typhoid fever
 If the fetus survives, it is born prematurely or
small for gestational age, with persistent failure to
thrive and manifestations of sepsis during the first
week of life.
 An abrupt onset with fever & vomiting.
TYPHOID IN INFANCY
 Typhoid fever during the first two years of life
presents an atypical picture.
 It may resemble that of septicemia or a
gastrointestinal disturbance.
 The temperature may be of the “septic spiking”
or “saw-tooth” type of fever, or it may be
irregular. The fever lasts about two weeks.
 Diarrhea may or may not be present; sometimes
there is constipation, or transient diarrhea
followed by constipation.
 Abdominal distention is an accompanying
manifestation. “Rose spots” and splenomegaly
are in frequently seen.
 Convulsions or meningeal signs are occasionally
encountered.
TYPHOID IN CHILDREN (above 2 years)
 Clinical manifestations of typhoid fever generally tend
to resemble those seen in the adult, although the
clinical picture is less severe and the mortality is low,
and the course is often short.
 After an INCUBATION PERIOD, of 8 to 14 days, the
initial stage may resemble an acute respiratory
infection, and the patient may present with a low
grade fever which may increase gradually to 40 to 41 C
or may continue as such.
 The temperature maybe intermittent with chilliness or
chills, and may recur in episodes with afebrile periods,
especially under non-specific treatment.
 DIARRHEA is a significant accompanying symptom
when present.
 ABDOMINAL PAIN with distention and tenderness,
and splenomegaly are common manifestations.
 Towards the end of the FIRST WEEK, “rose spots”
may appear and maybe seen in fair individuals.
 In some cases a typical skin manifestations in the form
of generalized maculopopular eruptions resembling
dengue, urticarial-like rashes or even petechiae maybe
noticed, which disappear in a few days.
 In the SECOND WEEK, the fever is sustained at a high
level and the pulse becomes more rapid.
 The characteristic “mental torpor” appears, and
disorientation or delirium maybe observed.
trans by: Lourdes L. Lorenzo Medicine
 Abdominal symptoms may become marked.
 In mild cases, the patient condition improves, but in
severe cases symptoms may persist and in the third
week manifestations of complications may be
observed.
Complications:
 Intestinal hemorrhage, perforation, and
peritonitis.
 Hepatitis with jaundice may occur and rarely
spontaneous rupture of the spleen.
 Respiratory complications including pneumonia
may result from concomitant gram-positive
infection.
 Otitis, arthritis, osteomyelitis, nephritis,
meningitis, or nervous system manifestations as
encephalitis or psychosis may also be seen.
 Particularly important in infants is fluid and
electrolyte imbalance.
Laboratory Data
 LEUKOPENIA is usually observed in children.
 Blood, stool and urine culture are almost always
positive during the first week and are definitely
diagnostic.
 Bone marrow cultures give a high frequency of
positive isolation at any stage of the disease.
 The WIDAL TEST which is a serologic test for
Salmonella agglutinis may suggest the diagnosis of
Salmonella typhi infection but this has been
shown to lack specificity and sensitivity and should
therefore not be used to make diagnosis.
Diagnosis.
 A typical course of typhoid fever in infants and young
children makes diagnosis somewhat difficult.
 The presence of diarrhea may make it necessary to
differentiate the disease from shigellosis.
 Any fever lasting for a week or more and which resists
usual management should arouse a strong suspicion of
typhoid.
 Blood and stool cultures should be performed for
definitive diagnosis.
Prognosis.
 The mortality rate in typhoid fever is low provided
early diagnosis and management are made.
 Prophylaxis, Hygienic and public health measures are
important in the prevention of the disease
 It may be done at yearly intervals. Immunization
reduces the risk of active disease.
Page 25 of 39
Current immunization:
 Includes a parental inactivated vaccine, given
subcutaneously
 A Vi capsular polysaccharide, administered
intramuscularly
 Oral vaccine with Salmonella typhi strain Type 21A.
Treatment:
 Drug of choice against typhoid fever continues to
be CHLORAMPHENICOL, although resistance
strains have been reported.
 In children: CEFTRIAXONE is the drug of
choice for multi drug resistant typhoid.
 AMOXICILLIN or AMPICILLIN at
100mg/kg/day or more may also be used if
sensitivity is shown.
 the combination TRIMETHORPIN –
SULFAMETHOXAZOLE is another effective
medication, alone or combined with
CHLORAMPHENICOL in severe cases.
Clinically, observable response may take 3 or 4
days.
 Steroids have been shown to shorten the febrile
course and hasten improvement; they may also
be indicate in severe cases.
 Non-typhoidal Salmonella infections usually
require only SUPPORTIVE CARE. There is
substantial evidence that the use of antibiotics
prolong the convalescent carrier state
 AMPICILLIN is recommended for the
prematures and newborn.
 carriers maybe given TRIMETHOPRIM-
SULFADIAZINE or SULFAMETHOXAZOLE for
bacteriological clearance of the inapparent state.
 electrolyte balance, proper nutrition and blood
transfusion are among the importance supportive
measures.
SHIGELLOSIS
 Acute diarrheal syndrome with bloody or mucus
containing tools associated with dehydration, systemic
sign of toxicity, and neurologic manifestation.
Etiology and Epidemiology:
 The genus Shigella is a group of slender non-motile
gram-negative rods which are mostly non-lactose
fermenters.
 Classified into FOUR SEROLOGIC GROUPS with 39
serotypes based on the antigenic characteristics
of their cell wall: These are:
1. S. dysenteriae (Group A).
2. S. flexneri (group B)
3. S. boydii (Group C) and
4. S. sonnie (Group D).
trans by: Lourdes L. Lorenzo Medicine
 In the Philippines, the most common is
S. flexeneri followed by S.sonnie
 S. dysenteriae is the classic agent of invasive
diarrhea and can cause very severe illness and
death untreated cases can be as high as 20%.
 Their habitat is almost exclusively the lower
gastrointestinal tract of humans. Like other
gram-negative bacilli, they possess a resistance
factor against antibiotics.
 The spread is through fecal-oral route and
contamination occurs thru improper handling of
food, unhygienic stool disposal, or transmission
through insect vectors.
 It is common in places with overcrowding and
poor environmental sanitation.
 The highest incidence occurs in children between
1 and 4 years and is rare below 6 months of age.
Pathogenesis and Pathology.
 Shigella multiply after the initial invasion of the
epithelial cells of the colonic mucosa resulting in
inflammation and ulceration. An endotoxin called the
Shiga cytotoxin is produced which inhibits protein
synthesis within the cell, responsible for the DIFFUSE
ACUTE COLITIS and ulceration that follows. There is
subsequent crypt distortion and blockage leading to
development of crypt absesses. The presence of
enterotoxin probably stimulates jejunal secretion of
fluids. The small intestine is usually not involved in the
disease process.
Clinical Manifestations:
 INCUBATION PERIOD varies from 3 to 7 days for
S. dysenteriae and 1 to 3 days for the other strains.
 Characterized by:
 an acute onset of malaise,
 fever,
 crampy abdominal pain followed by diarrhea
of a watery or pastelike consistency,
 tenesmus and
 urgency.
 Within 48 hours, stools could become bloody or
mucus-containing and small in amount. Bowel
movement is most frequent during the first 24 hours
and gradually decreases.
 Physical examination may reveal:
 abdominal tenderness,
 hyperactive bowel sounds and
 mild to severe dehydration
 Neurologic manifestation such as seizures
lethargy and drowsiness may occur in 10 to
45% of children.
 Sigmoidoscopy may reveal intense hyperemia,
multiple small beeding sites, loss of transverse mucosal
folds and formation of pseudomembranes.
Page 26 of 39
Diagnosis:
 Patients with bloody diarrhea should be presumed to
have Shigella and treated with an antimicrobial to
which it is sensitive.
 Stool cultures may be necessary in cases of bloody
diarrhea or when the clinical manifestation of high
fever, toxicity or seizures appear in these patients.
 The presence of polymorphonuclears in the stools
may also be suggestive of this invasive pathogen.
 Other enteropathogens that can give rise to
bloody diarrhea are:
 Campylobacter jejuni
 Yersinia enterocolitica
 Enteroinvasive E. coli and
 Entamoebahistolytica.
Treatment:
 In the Philippines, the currently recommended, most
cost effective antimicrobial for Shigella is
COTRIMOXAZOLE.
 Alternative drugs are NALIDIXIC and
CHLORAMPHENICOL. Sensitivity testing is
necessary in areas with high resistance.
 Parentral or oral rehydration with electrolyte
correction are important supportive measures.
Also included are antipyretics and
anticonvulsants when indicated.
Prognosis.
 Mortality is high in untreated cases with reports of
the development of hemolytic-uremic syndromes
both in children and adults.
Prevention.
 Good sanitation and hygienic practices should
be emphasized together with provision for clean
water supply.
 Handwashing after defecation is important to
prevent transmission.
 Effective vaccines have not yet been developed.
Pathogenesis and Pathology:
CHOLERA
 Characterized by massive loss of fluids resulting
in rapid dehydration and shock.
 Diarrhea is caused by the vivo production of
enterotoxins which stimulates the internal
secretion of fluids and electrolytes. Death from
dehydration, acidosis and circulatory collapse
occurs in untreated cases
trans by: Lourdes L. Lorenzo Medicine
Etiology:
 1883 Robert Koch first isolated the organism
Vibrio cholera from the stool of patients
suffering from the disease. It is a gram-
negative, curved bacillus that is highly motile
by means of a single flagellum. It needs a
selective medium, the thiosulfate-citrate-bile-
sucrose (TCBS) agar to facilitate isolation and
laboratory diagnosis.
 Two biotypes of Vibrio cholera are re-
organized:
1.) the classic and
2.) El Tor vibrio.
 Each biotype can exhibit Ogawa or Inaba
specificity such that 4 distinct types of Vibrio
cholera are identified.
 The differentiation is based on agglutination
reactions and grouping is according to their O
somantic antigens with Group O being the
usual cause of clinical cholera.
 The disease is spread rapidly by means of
fecal contamination of water, milk and other
foods.
 The organism survives well at ordinary
temperatures and longer in refrigerated
foods.
 Animal vectors are not considered important
in its transmission.
 Children are usually more severely affected
with about 24% occurring below 5 years and
10% below 2 years.
 ADULTS have preexisting vibriocidal and
antitoxin antibodies from previous
infections.
 Breastfeeding in children appears to be
protective against cholera because of
antibodies found in breastmilk.
 The organism after adhering to the epithelium
multiply and produce an enterotoxin
(choleragen) which binds to receptor on the
surface of the cell and activities intracellular
adenelatecyclase to convert adenosine
triphosphate (cAMP).
 Increased cAMP activates a secretory
mechanism which block sodium absorption and
promotes secretion of water chlorides.
 The toxin acts through an intact epithelium on the
vasculature of the bowel with resultant
outpouring of intestinal fluids.
Page 27 of 39
  The intestinal mucusa is congested but
unaltered, with hypertrophy of lymphoid tissue.
 There is an inflammatory reaction in the lamina
propria of the bowel characterized by
engorgement of the capillaries.
 Dilation of the central lacteals, and a cellular
infiltrate composed mainly of mononuclear cells,
plasma cells, lymphocytes and histiocytes.
Clinical Manifestations:
 INCUBATION PERIOD is 2 to 3 days.
 Characterized by sudden onset of profuse watery
diarrhea accompanied by severe vomiting and
abdominal cramps.
 Stools are whitish to greenish slightly mocuid
without any fecal matter, so called “rice-water”
stools, with a peculiar somewhat fishy odor.
 At the outset, stools are passes repeatedly, later
becoming almost continuous without straining or
tenesmus.
 Signs of severe dehydration: occur rapidly,
such as:
 sunken fontanels and eyeballs,
 prominence of sutures,
 loss of turgor and elasticity of the skin
 positive skin fold sign with wrinkling of the
fingertips
 There is oliguria and even anuria.
 Fever may be low grade or moderate at the start,
but become subnormal in later stages.
 Tetany, abdominal distention, encephalitis like
symptoms and convulsions may occur,
particularly during the rehydration phase similar
to those of the post-acidotic phase of infantile
diarrhea.
 The THREE PRINCIPAL DEFICITS during cholera
giving rise to manifestations are:
1. Severe dehydration and extracellular volume
loss leading to shock,
2. Acidosis which produces Kussmaul
respiration, and
3. hypokalemia which may manifest as
distention due to paralytic ileus as well as
during the rehydration or post acidotic phase
of treatment .
Laboratory Data:
 There is a hemoconcentration with elevated
hemoglobin levels, marked metabolic
acisodis, and hyperelectrolytemia particularly
potassium.
 Blood plasma specific gravity is ELEVATED.
trans by: Lourdes L. Lorenzo Medicine
Diagnosis:
 Isolation of the organisms from the stools will
establish the diagnosis.
Complications:
 ACIDOSIS & SHOCK are common complications.
 Hypocalcemia and hypokalemia frequently
follow acidosis.
 Renal failure and uremia due to tubular
necrosis may occur, as well as respiratory
complications like pneumonia.
Prognosis:
 The mortality rate is low by prompt and vigorous
fluid and electrolyte therapy, but remains high in
the young and undernourished individuals.
Prophylaxis:
 Patients with cholera or suspected cases should
have enteric isolation procedures.
 Disinfection` or boiling of water will prevent
transmission of cholera as well as thorough
cooking of food.
 Appropriate handwashing after defecation and before
food preparation or eating is important in preventing
transmission.
 Prophylactic treatment is not recommended UNLESS
unusual sanitary and hygienic conditions indicate that
the rate of secondary transmission maybe high.
 The administration of TETRACYCLINE, DOXYCYCLINE
or TRIMETHOPRIM-SULFAMETHOXAZOLE within
24 hours of identification of the index case may be
effective in prevention.
Treatment:
 The water and salt lost in the cholera stool must be
replaced in comparable amounts and concentration.
 Early replacement decreases the chance for
complications secondary to severe volume depletion
to occur
 This replacement can be done by mouth with the use
of packets of salts and a carrier substance, like the ORS
of the WHO formulation to mix with a given volume of
water, which should be given as soon as possible to
prevent the progression of dehydration to serious
clinical levels.
 Recently it has been shown that the RICE can
substitute for glucose or sucrose as carrier substance
in an effective ORS. The rice solution significantly
reduced stool output during the first 24% by 36% in
adults and by 32% in children with cholera. In non-
cholera patients, reduction of stool output by rice ORS
is only 18%.
 Intravenous replacement is needed when
appropriate oral treatment has not been given and the
patient has gone into hypovolemic shock.
Page 28 of 39
  LACTATED RINGERS SOLUTION has been found
preferable to the standard fluid (3 parts NSS and 1 part
2% sodium bicarbonate solution) for pediatric
treatment as it supplies the needed ion replacement
and does not give rise to untoward manifestations
during the period of therapy, markedly diminishing the
incidence of complications of mortality.
 Complications like shock, hypokalemia and
hypocalcemia are managed accordingly.
 Antibiotics shorten the duration of diarrhea and
therefore decreases fluid losses in cholera.
 TETRACYCLINES and its congeners are the drugs of
choice in most instances. The recommended dosage is
12.5 mg/kg body weight 4x a day for 3 days.
 Alternatives are:
 FURAZOLIDONE at a dose of 1.25mg/kg body
weight 4x a day x 3 days or
 TRIMETHOPRIM at 5 mg/kg body weight and
SMX at 25 mg/kg body weight 2x a day for 3 days.
ESHERICHIA COLI INFECTIONS
 Particularly incriminated in the diarrhea of newborns
and infants, especially those in epidemic forms in
sepsis and meningitis of the newborn, and in urinary
tract infections.
 Although they are normally found in the intestines,
some particular strains have been proven pathogenic.
 Diarrheagenic or enteropathic strains fall under
TWO CATEGORIES:
1.) the ENTEROTOXIGENIC and
2.) the ENTEROINVASIVE dysenteric type stools.
 Recently, a strain of E. coli (055:K59:H4) which
produces a CYTOLETHAL distending toxin has been
reported to produce gastroenteritis and
encephalopathy with disturbances of cardiovascular,
neurologic and hepatocellular function mediated by
this toxin.
 Most of the acute urinary tract infections in infants
and children are produced by E coli with colony counts
of 100,000 organisms or more per mL of specimen.
 The STOOLS in the enterotoxigenic infections are
watery, colorless or greenish, foul, explosive and
abundant;
 Those in the INVASIVE TYPE are bloody mucoid with
plenty of cellular elements.
 Dehydration and electrolyte imbalance are
prominent particularly in the enterotoxigenic type,
which is often accompanied by vomiting.
 E. coli sepsis in the newborn may start vaguely with
anorexia, fretfulness or lassitude.
trans by: Lourdes L. Lorenzo Medicine
 Fever, jaundice, diarrhea and anemia are more
definite symptoms. Hemorrhagic manifestations may
appear in severe cases.
 E. coli serotype 0157:H7 is a known cause of
HEMORRHAGIC COLITIS and HEMOLYTIC-UREMIC
SYNDROME, the new terminology still being
undetermined. Dairy cattle are a reservoir of the
strain.
PSEUDOMONAS INFECTIONS
 Pseudomonas and related species are gram-negative
aerobic rod belonging to the family Pseudomonaceae.
They are motile non-spore forming.
 The most important of the opportunistic
pseudomonads is Pseudomonas aeruginosa.
 P. aeruginosa are effective agents in the newborn
nurseries, particularly among premature, in
malnourished children, in those receiving therapy with
other antibiotics and immunosuppressive drugs, and in
burns and in neurosurgical patients.
 Pseudomonas septicemia is associated with high
morbidity and mortality
 P. aeruginosa can also cause:
 endocarditis corneal infection,
 otitis externa,
 mastitis,
 mastoiditis,
 meningitis,
 pneumonia,
 peritonitis and
 urinary tract infections.
 Sources of Other pseudomonads that cause other
diseases include Burkholderiapseudomallet which is
the causative agent of malioidosis and are most
prevalent in tropical and subtropical areas of Southeast
Asia and Northern Australia.
 Burkholderiacepacia which is usually multidrug
resistant.
 Stenotrophomonasmaltophilia (formerly
Xanthomonasmaltophilia) has been identified as a
cause of sporadic nosocomial outbreaks of infection in
medical intensive care units (MICU).
Diagnosis:
 Depends on recovery from the blood, cerebrospinal
fluid, and urine not contaminated by the cuntaneous
flora.
 Recovery of the organism from the surface of the skin
or, bronchial secretions may reflect colonization and is
not necessarily diagnostic of infection
 Nosocomialy acquired P. aeruginosa is more likely to
be antibiotic resistant than community acquired
strains.
 The combination of an Aminoglycoside and Beta
lactam antibiotic is synergistic against the organism.
Page 29 of 39
  The antibiotics for treating P. aeruginosa and other Table 14.5 ANAEROBIC BACTERIA RESPONSIBLE FOR
Pseudomonas infections are based on the current CLINICAL INFECTION
sensitivity patterns are CEFTAZIDIME, IMIPENEM Gram positive
and AMIKACIN. Cocci
 Intrathecal administration of AMIKACIN is advocated Peptostreptocococci
for complicated central nervous system infection Microaerrophilic
for the first few days. Streptococcus
Bacilli
Clostridium species
ANAEROBIC INFECTIONS Eubacterium
 Anaerobic bacteria are important because they
Propionibacterium
dominate the indigenous flora and some of those
Porphyromonas species
infections are serious and have a high mortality rate.
Fusobacterium species
Gram negative
CNS Infections Cocci
 Anaerobic organisms play a role in intracranial Veillonella
infections either as principal or as contributing agents. Bacilli
This is a particularly true for brain abscess which Bacteroides fragilis
usually occurs in the setting of patients with chronic Prevotellamelaninogenica
otitis, mastoiditis, or sinusitis or in children with and related species
cyanotic congenital heart disease.
 Until bacteriologic results are available a combination OSTEOMYELITIS.
of METRONIDAZOLE with GENTAMYCIN or  Long bones maybe infected via hematogenous route,
AMPICILLIN could cover for all presumptive during surgical placement of a foreign body, or by
pathogens. superinfection
 In general the clinical features of anaerobic infections
ORAL Infections: is similar to that caused by facultative organisms. The
 Bacteroides, Fusobacteriaans Veillonella species major clinical distinction, when present, is the foul
are normal inhabitants of the oropharynx, in the odor associated with anaerobic infection.
tonsillar crypts of the tongue plaque forming on the  Radiographs demonstrating gas is infected tissues
surfaces of the teeth, and gingival crevices. maybe helpful but are non-specific.
 It is associated with infections such as dental  The treatment of anaerobic infection usually involves
abscesses or gingivitis. Most of these are sensitive to appropriate debridement and antibiotic therapy.
PENICILLIN.
LEPROSY
SKIN:  Chronic disease with an insidious onset, transmitted
 On the skin, genus propionibacterium is the most from man to man with protean manifestations
prevalent among them are the: affecting the skin, mucous membranes, nervous tissue
 P. aenas and eventually producing physical deformities
 P. granulosum and
 P. avidum. Etiology and Epidemiology.
 The disease is characterized by a host-parasite
LOWER RESPIRATORY TRACT Infections relationship and is caused by Mycobacterium
 These are THREE MAIN TYPES of pathology produced: leprae, an intracellular, low virulent, acid fast bacilli
1.) pneumonia  There is direct transmission in man mainly through
2.) necrotizing pneumonias inhalation and is neither hereditary nor congenital.
3.) lung abscesses Essential for its transmission are a probable genetic
 These mostly follow aspiration of material from the susceptibility and an intimate prolonged contact with
oropharynx, which produces infection in the basal an infectious case.
region of the lungs.  Other risk factors are:
 low-socio-economic status,
ABDOMINAL infections:  poor nutrition,
 Anaerobic bacteria are isolated most frequently from  crowding,
children with peritonitis cause by appendicitis or  dirt and poor hygiene
gastrointestinal perforation.

trans by: Lourdes L. Lorenzo Medicine Page 30 of 39

  Recent studies have not shown any significant impact Diagnosis.
on the incidence of leprosy among populations with a  The BASIS OF DIAGNOSIS of the disease are the
high prevalence of positive HIV. following:
1. CLINICAL; which can show systemic,
Pathology and Pathogenesis skin or pheriperal nerve involvement
 A widely disseminated lepromatous lesion occurs 2. MICROBIOLOGIC; demonstrating the
when the patient’s immunologic mechanisms are organism in the skin or mucosa
incapable of mounting an immune response. 3. HISTOPATHOLOGICAL: showing formation of
 This can be assessed by an intradermal injection of a foamy cells, where the bacilli invade and destroy
prepared suspension of killed M. leprae from the histiocytes or the formation of tuberculoid
lepromatous tissue. granuloma where the baccili are phagocytosed
 A highly positive test (induration) is indicative of and destroyed by macrophages
TUBERCULOID, a weak or negative reaction is 4. IMMUNOLOGIC; based on the LEPROMIN TEST
lepromatous and an intermediate is seen a using a positive or negative MITSUDA REACTION.
Tuberculoid, borderline and lepromatous
borderline cases. This is the so called MITSUDA
classification are used in general (Madrid – Ridney-
REACTION.
Jopling) but WHO uses the categories of
 Lesions are mainly in the skin, peripheral nerves and
paucibacillary and multibacillary types.
mucosa of the upper respiratory tract.
 The M. leprae proliferate in the Schwan cells of the  Diagnosis of leprosy is thus mainly based on
nerves and produce foamy degeneration of the axon, characteristic skin lesions, sensory loss, thickening of
with marked fibrosis and destruction of normal the nerve trunks and the presence of acid fast
structure. Lepromatous nodules contain large, organism in the skin smears.
lipiladenmacrophages and giant cells filled with  COMPLICATION in leprosy include reversal reaction
and erythema nodosumleprosum.
bacilli (Virchow’s lepra cells) or there are
microscopic granulomas resembling hard tubercles. Treatment:
 Vascular changes and secondary infections lead to  WHO recommends the treatment of leprosy to be
necrosis, suppuration and ulceration. based on the administration of a combination of
 Cell mediated immunity (CMI) seems to play a large drugs, referred to us Multi-Drug therapy (MDT)
part in the production of leprosy lesions. which for multibacillary leprosy consists of:
 CMI to M. leprae is makedly suppressed in the  RIFAMPICIN
lepromatous patient.  CLOFAZIMINE
 DAPSONE.
Clinical Manifestations.  For paucibacillary:
 The INCUBATION PERIOD is variable, from 2 to 5  RIFAMPICIN and DAPSONE are the
years or more with the appearance of cutaneous recommended combination.
lesions dependent primarily on the cell-mediated  The treatment of complications such as reversal
immune response of the host to M leprae. reaction and erythema nodosumleprosum
 The indeterminate (T) lesion which may be initial essentially involves the use of PREDNISONE.
manifestation shows ordinary-looking skin changes  The DURATION OF TREATMENT is given for a long time
such as pale, oval or rounded macules,
i.e. 6 months for paubacillary and 2 to 5 years
papulonodules, wheals or circinate patches. They
until smears are negative for multibacillary.
may be found in the malar area, extremeties or
buttocks. Prevention:
 The lesions are usually anesthetic but this may be a  While leprosy is a major problem in many countries,
later manifestations. They may be depigmented or and an effective vaccine is still to come, improvement
erythematous. Sensory disturbances as paresthesias, of public health methods appears to be in addition to
numbness and formication may also be found. Any of antileprosy drugs, the most meaningful solution.
the above six forms maybe found as initial
manifestations of the disease. Table 14.7 INITIAL LESIONS AT DOVERY BY AGE GROUPS
0-4 5-9 10-14 Total
M F M F M F
Tuberculoid 4 7 70 51 136 105 373
Borderline 3 0 32 21 81 46 183
Lepromatous 0 0 23 10 86 43 162
Indeterminate 5 1 18 19 13 20 76

trans by: Lourdes L. Lorenzo Medicine Page 31 of 39

LEPTOSPIROSIS Etiology and Epidemiology
 This is an acute systemic infection that follows contact  At least 180 pathogenic serotypes of leptospires.
with:  RODENTS are the most important reservoir but virtually
 blood all mammals may be infected and can transmit the
 urine disease.
 tissues  The organisms can survive outside the animal hosts if the
 organs of infected animals environmental condition is favorable and may survive
 exposure to an environment that has been longer than 3 weeks in stagnant waters.
contaminated by leptospires  In the Philippines, 4 to 5% were positive for leptospira
 The organisms enter breaks in the skin or penetrate the antibodies but where in those more than 20 years of age.
mucus membranes including conjunctiva, nasopharynx or  L. pyogenes and L. manila were the most commonly
vagina. found strains. Other species were:
 L. icterohemorrhagicae,
 L. canicola,
 L. batavia,
 L. pomona
 L. javanica.

trans by: Lourdes L. Lorenzo Medicine Page 32 of 39

Pathology
 After the organism penetrates the skin and mucus
membrane, leptospires invade the bloodstream and
spread throughout the body such as the outer chamber of
the eye and subarachnoid space.
 Pathologic manifestations are usually due to direct injury
by the organism, presence of edotoxins that damage the
RBC and hepatocytes and the immune response of the
body against the organism.
Clinical Manifestation
 ACUTE SYMPTOMS:
 Extensive vasculitis varying in severity from
asymptomatic to a fatal outcome
 THREE STAGES of the disease may be recognized:
1. septicemic or febrile
2. Immune or toxic with or without jaundice
3. Convalescence
 Clinical course follows a BIPHASIC COURSE:
STAGES:
1. SEPTICEMIC STAGE
 Duration: about 4 to 7 days
 Characteristics:
 fever
 myalgia
 headache
 abdominal pain
 vomiting
 conjunctival suffusion
 At the end of this stage, leptospires DISAPPEAR
from the blood and CSF
2. IMMUNE PHASE
 Duration: 4 to 30 days during which
LEPTOSPIRURIA is prevalent affecting renal
functions significantly
 Characteristics: There is:
 diminution of fever with rash
 conjunctival injections
 headache
 meningeal manifestations, with CSF
findings of aseptic meningitis.
 IRITIS or IRIDOCYCLITIS are observed
at this stage.
 HEPATIC INJURY could also be
pronounced in some cases thus
producing the so called Icteric
Leptospirosis (Weil’s Syndrome).
 DEATH may occur between the 9th to 16thday of
illness.
 In 1977, oligoanuria was reported in 62.5% and
azotemia in 84.37% of cases
 Mortality was 34.4%. The immune phase, 88%
had acute renal failure with varying severity.
trans by: Lourdes L. Lorenzo Medicine
 Other manifestations include:
 hepatomegaly
 hyperbilirubinemia
 elevation of the transaminase levels, with shock
and congestive heart failure seen in severe cases.
Diagnosis
 Clinical picture + history of exposure = suggestive of the
disease
 Impaired hepatic and renal function tests:
 Albumenaria
 Hematuria
 Cylindruria
 During the SEPTICEMIC STAGE, the spirochetes may
be cultures from blood and CSF
 During the IMMUNE PHASE, the spirochetes may be
cultures from the urine
 Dark field microscopy is highly specific but low in
sensitivity as it will require 10,000 to 20,000
leptospires/mL of fluid for identification.
 Microscopic Agglutination Test (MAT)
most specific and reliable test for leptospirosis.
 Other serologic tests such as:
 compliment fixation
 indirect immunofluorescent test
 counter immunoelectrophoresis and
 ELISA have been utilized.
 False negative tests are usually due to presence of
another or unrecognized serotype if not included in the
test antigens, and if blood examination is done after
peaking of the titer and antibiotic suppression.
 Ellinghausen-McCullough-medium: can culture
leptospires from Blood, urine, CSF and other body fluids.
Local availability is limited.
Treatment
 PENICILLIN  drug of choice
 when given early can decrease:
 the duration of fever
 the incidence of jaundice
 meningismus,
 renal involvement and
 hemorrhagic manifestations.
 It can also prevent leptospiruria.
 TETRACYLINE  alternate drug
 Suppotive management is the mainstay of therapy as
the disease appears self-limiting.
 Fluids and electrolyte monitoring with blood
transfusion when indicated are necessary.
 In acute renal failure, peritoneal dialysis has often
been life saving.
Prevention
 Environmental sanitation remains to be the best control
measures for leptospirosis particularly the maintenance of
sanitary conditions in animal yards or confines.
 Animal immunization is also being done.
Page 33 of 39
SYPHILIS
Etiology
 Treponema pollidum  a slender, long, tighly
coiled, motile spirochete with finely tapered ends
belonging to the family Spirochaetaceae and genus
Treponema.
 The PATHOGENIC MEMBERS of this genus include:
 T. pallidum (syphilis)
 T. pertenue (yaws)
 T. carateum (pinta)
Epedimiology
 Syphilis occurs worldwide
 The incidence of both acquired and congenital syphilis
has remained low in the Philippines
 The Philippine Health Statistics has reported a
morbidity rate of 0.2 per 100,000 population and no
mortality for 1990.
 Congenital syphilis is acquired from an infected
mother via transplacental transmission of spirochetes
anytime during pregnancy or at birth.
 40% of pregnancies in women with untreated, early
syphilis result in spontaneous abortion, stillbirth or
perinatal death.
 In untreated syphilis, rate of transmission is almost
100% during secondary stage and slowly decreases
with increasing duration of disease.
 Transmission may occur throughout pregnancy but is
most likely in the third trimester.
 Acquired syphilis is contracted almost always
through sexual contact with ulcerative lesions of the
skin or mucosa of infected persons.
Clinical Manifestations
 EARLY (first 2 years of life)
 Variable but most often manifest during the first
few week or months of life
 Non-specific symptoms such as fever, failure to
gain weight, irritability and pallor may be present
 A vesicular or bullous or desquamative
maculopopular rash is characteristic on the hands
and feet but may become generalized.
 Wart-like moist lesions about the mouth, anus
and external genetalia may be present.
 A purulent or blood-tinged nasal discharge
(“snuffles”) is seen in 10% of cases.
 These mucocutaneous lesions are teeming with
spirochetes.
 Hepatosplenomegaly (30%),
hyperbilirubinemia and elevated liver enzymes
are common.
 Lymphadenopathy (5%)
trans by: Lourdes L. Lorenzo Medicine
 Bone involvement (25%) occurs as
 OSTEOCHONDITIS at the wrists, elbows,
ankles and knees;
 PERIOSTITIS of long bones;
 widened and serrated epiphyseal lines and
separation of epiphysis.
 Thrombocytopenia and leucocytosis are
frequent.
 Immune-complex glomerulonephritis (5%)
may be noted.
 Among the 8 cases of congenital syphilis admitted
at the Philippine Children’s Medical Center,
majority presented with:
 jaundice
 abdominal distention and
 pallor
 but there were no roentgenographic
abnormalities seen.
 It must be differentiated from other generalized
congenital infections like tuberculosis, rubella,
herpes simplex, cytomegalovirus and
toxoplasmosis; bacterial sepsis; other skin
infections like staphylococcal impetigo, scalded
skin syndrome, scabies and diaper moniliasis.
 LATE (appear gradually during the first 2 decades)
 The manifestation result from chronic inflammation
of bone, teeth and the central nervous system.
 Skeletal changes include frontal bossing
(“Olympian brow”)
 Anterior bowing of the midportion of the tibia
(saber shin)
 Scaphoid scapula
 Dental abnormalities include Hutchinson’s teeth,
abnormal enamel and mulberry molars.
 Other manifestations are:
 saddle nose
 perforated nasal septum
 rhagades
 juvenile paresis
 interstitial keratitis
 eight nerve deafness and
 Clutton’s joints.
Diagnosis
 The organism cannot be cultured in vitro and
laboratory isolation requires animal inoculation.
 Definitive diagnosis: identification of spirochetes by
microscopic darkfield examination or direct fluorescent
antibody test of lesion, exudates or tissue.
 Specimens from mouth lesions require direct
fluorescent antibody techniques to distinguish T.
pallidum from non-pathogenic treponemes.
 Placental examination by gross and microscopic
techniques is useful in the diagnosis of congenital
syphilis.
Page 34 of 39
  Presumptive diagnosis
 2 types of serologic tests:
1.) NON-TREPONEMAL TESTS:
 VDRL slide test
 Rapid plasma reagin (RPR) test
 Automated reagin test (ART).
 Measures IgG and IgM antibody against a
nonspecific lipoidal antigen (“cardiolipin”)
from T. pallidum and/or its interaction with
host tissue.
2.) TREPONEMAL TESTS  maybe falsely
negative in early primary, latent acquired and
late congenital syphilis.
 Routine serologic testing for syphilis is
recommended during the FIRST TRIMESTER and PRIOR
to delivery in high-risk populations.
 Treatment is indicated when clinical findings or
serologic findings suggest active infection.
 No alternative is proven for PENICILLIN!!!
 Allergic patients and pregnant women should be
treated with PENICILLIN after desensitization.
 The Jarisch-Herxheimer reaction  an acute
febrile reaction, may occur in 15-20% of patients
with acquired or congenital syphilis who are
treated with PENICILLIN. It is not an indication to
discontinue PENICILLIN therapy.

 FALSE POSITIVE results can be caused by:

 infectious mononucleosis
 connective tissue disease
 TB
 endocarditis and
 abuse of injectable drugs.
 Maternal antibody crosses the placenta, and
accordingly a false-positive VDRL can occur
in an uninfected infant delivered to a VDRL-
positive mother.
 Passively acquired antibody is suggested
when neonatal titers are significantly less (4-
fold or less) than maternal titers and can be
verified when antibody is no longer
demonstrable by 3 months of age.
 False negative test results may occur in
infants who acquire infections late in
pregnancy; such infants become seropositive
in the postnatal period.
 Neither type of test alone is sufficient for
diagnosis LESS COMMON BACTERIAL INFECTIONS

CEREBROSPINAL FLUID TESTS Arcanobacterium Hemolyticum

 CSF should be examined in infants born to mothers with
syphilis during pregnancy
 The RPR, FTA-ABS, and MHA-TP tests should not be used
for CSF evaluation.
 CSF VDRL test results should be interpreted cautiously since
a negative VDRL does not exclude neurosyphilis and the
CSF VDRL can be positive in an uninfected newborn with a
transplacentally acquired, high serum VDRL titer.
Treatment and Prevention
 Parenteral PENICILLIN G preferred drug at any stage
 Infants should be treated for congenital syphilis if:
 they have physical or roentgenographic evidence of
active disease; or
 their serum VDRL or RPR is reactive; or
 their CSF VDRL is reactive or CSF cell count and/or
protein concentration is abnormal.
Infections
Etiology
 Arcanobacterium hemolyticum  is a gram-positive
bacillus, formerly termed Corynebacterium hemolyticum
Epidemiology
 It is only rarely isolated from animals and its primary
epidemiologic reservoir appears to be human since the
organism may be found in the pharynx and skin of healthy
humans.
Clinical Manifestations
 Acute pharyngitis is indistinguishable from group A
streptococcal pharyngitis.
 It is associated with a “scarlatiniform rash” that begins in
the extensor surfaces of the distal extremities and spread
centripetally.

trans by: Lourdes L. Lorenzo Medicine Page 35 of 39

  There are NO palatal petechiae, strawberry tongue or post Treatment
infectious complications.  ERYTHROMYCIN should be given for 5-7days
 Skin infections include chronic ulceration, cellulitis, wound  It shortens the duration of illness and prevents
infection and paronychia. relapse if given early
 Rare infections are vertebral osteomyelitis, septicemia,  CIPROFLOXACIN - alternative drug
brain abscess and endocarditis.
Prevention
Diagnosis  Enteric precautions, hand-washing after handling raw
 The organism grows on sheep blood agar with beta- meat, thorough cooking of poultry, pasteurization of milk
hemolysis. and chlorination of water supplies are all important.
 Serologic tests are not available commercially.
Legionella Pneumophila Infections
Treatment
 ERYTHROMYCIN  drug of choice Etiology
 Legionella are fastidious, weakly staining, gram-negative,
Prevention: none rod-shaped or filamentous bacilli.
 UNIQUE FEATURES: presence of DNA, cellular fatty acid,
Campylobacter Infections and their dependence for growth on L-cysteine on
primary isolation
Etiology  23 different known species as of 1987 but L. pneumophila
 Campylobacter jejuni (formerly Campylobacter fetus) type I is largely responsible for human disease
 a motile, comma shaped, gram-negative bacillus that Epidemiology
causes gastroenteritis.  Legionnaire’s disease is acquired through inhalation of
 Campylobacter fetus (formerly C. fetus subspecies aerosolized water contaminated with Legionella
intestinalei), a related organism, is an infrequent cause of  Outbreaks were associated with exposure to contaminated
sepsis in neonates and debilitated hosts. airconditioning cooling towers, condensers and potable
water systems occurring in hotels, hospitals and large
Epidemiology building (L. pneumo)
 Reservoir of infection is the GIT of domestic birds, farm Clinical Manifestation
animals, pet dogs and cats.  Infection in children is uncommon and is usually
 Main vehicles  improperly cooked poultry, untreated asymptomatic or mild or unrecognized
water and unpasteurized milk  It is an important cause of adult pneumonia
 Person-to-person transmission has caused nosocomial  AT RISK:
nursery outbreaks  with chronic illness
 immune deficiency or
Clinical Manifestation  those receiving corticosteroids
 INCUBATION PERIOD: 1-7days  2 DISTINCT SYNDROMES:
 SYMPTOMS: 1. Legionnaire’s disease (pneumonia)
 bloody diarrhea  may manifest as:
 abdominal pain  mild respiratory disease, to sever multisystem
 fever with or without convulsions disease with GI, CNS, renal and
** abdominal pain can mimic appendicitis  progressive pulmonary symptoms
 COMPLICATIONS that can occur during convalescence 2. Pontiac fever
include:  has an abrupt onset, self-limited influenza-like
 Reactive arthritis illness without pneumonia
 Guillain-Barre syndrome Diagnosis
 Reiter’s syndrome  DEFINITIVE: recovery of the bacterium from respiratory
 Erythema nodosum tract secretions using direct immunofluorescence or
Diagnosis DNA probes
 Gram stain or darkfield microscopy  identify  Serology
organism from stool specimen  ELISA
 C. jejuni can be cultured from the feces and occasionally  Radioimmunoassay  allow rapid detection of
from the blood L. pneumophilaserogroup 1 antigen in urine
 Immunofluorescence antibody assay (IFA)

trans by: Lourdes L. Lorenzo Medicine Page 36 of 39

Treatment CHLAMYDIAL INFECTIONS
 DOC: ERYTHROMYCIN (30-60mg/kg/day) initially IV q
6hrs and changed to oral therapy once the patient Etiology
improves clinically.  Although previously considered as large viruses sensitive to
 RIFAMPIN (15mg/kg/day) for 3 weeks  may be added to antibiotics
patients who do not respond promptly to erythromycin.  Now known to have definite cell wall and two nucleic acids
similar to gram-negative bacteria
 Obligate intracellular, multiply via binary fission
Prevention
 3 SPECIES:
 Hyperchlorination and /or superheating to 70˚C with
1.) C. trachomatis
appropriate mechanical cleaning are effective in controlling
 has 15 serovars, w/ glycogen, stains w/ iodine, and
common-source outbreaks.
sensitive to sulfonamides.
 Vaccine for high risk patients may be feasible
 They have man as natural host and vertical
transmission is the rule.
Helicobacter pylori Infections  Can cause:
 pneumonitis of NB
Etiology  lymphogranulo-mavenereum
 H. pylori (formerly Campylobacter pylori) are gram-  hyperendemic blinding trachoma
negative spirally curved or U-shaped micro-aerophilic bacilli  inclusion conjunctivitis
that have a tuft of flagella at one end  non-gonococcal urethritis
 cervicitis
Epidemiology  salpingitis
 proctitis
 RESERVOIR: human and other promates
 epididymitis
 ROUTE OF TRANSMISSION: unknown
 Low in children, low socioeconomic groups and developing
2.) C. psittaci
countries  atleast 4 avian serovars, no glycogen and does not
stain w/ iodine.
 Resistant to sulfonamides and is a zoonotic
Clinical Manifestation infection w/ aerosols as mode of transfer. Cause
 INCUBATION: unknown
psittacosis.
 ACUTE: epigastric pain, nausea, vomiting, hematemesis
and guaiac-positive stools
3.) C. pneumonia
 1 serovar, no glycogen, resistant to
 Course is short but some develop gastric ulcers
sulfonamides and have human reservoir.
 PROLONGED: at risk for gastric adenocarcinoma
 Mode of Transmission respiratory secretions in all
ages.
Diagnosis  All specie cause pneumonia in infants & children!
 Gastric biopsy specimen: cultured in chocolate agar or
skirrow’s medium at 37˚C
 Urease testing of gastric specimen  rapid
Epidemiology
 Infection is not uncommon in infants & children but the
 Visualized with gram, hematoxylin-eosin, silver or Giemsa
incidence vary from location
stains
 Serologic test  detect antibody to H. pylori  C. trachomatis  most common bacterial STD
 Common in children less than 5 years of age
Treatment Neonatal Inclusion Conjunctivitis
 Triple therapy with AMOXICILLIN, METRONIDAZOLE
 Inclusion conjunctivitis (inclusion blenorrhea)
and BISMUTH SUBSALICYLATE  most effective
 usually acquired during passage through the birth canal.
 Usually after 1st week of life but some occur as early as the
Prevention 1st day esp. w/ PROM
 Disinfection of gastroscopes  Application of Crede’s prophylaxis has NO EFFECT!

Epidemiology
 Prevalence: 1.1-4.4/1000 live births
 40-50% infants born to infected women are found to
develop mild to moderate conjunctivitis positive for
Chlamydia

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Clinical Manifestation
 Thick mucopurulent eye discharge w/c tends to resolve
spontaneously within weeks to several months after onset
 Pseudomembranes may develop in conjunctiva with
resulting scarring in severe cases
 Chronic conjunctival infection is known to occur despite
treatment with development of scarring and corneal
vascularization
Diagnosis
 Tissue Culture or direct fluorescent antibody or enzyme
immunoassay methods
 Highly indicative-intracellular inclusion bodies in
conjunctival epithelium via Gemsa stain
Treatment
 Topical TETRACYCLINE or ERYTHROMYCIN ophthalmic
ointment within 1st hour of life can prevent
conjunctivitis but is not adequate for resolving
nasopharyngeal colonization nor preventing pneumonia
 Oral ERYTHROMYCIN 50mg/kg/day in 4 divided doses for
14 days
 SULFONAMIDES  alternative
 Treatment of chlamydia infection in pregnant women
 best method of preventing chlamydia ophthalmia
Chlamydial Pneumonia
 NBs with infected mothers  50-70% chance of acquiring
the organism that can persist for 3yrs
 Nasopharyngeal colonization, conjunctiva, rectum and
vaginal colonization.
Clinical manifestation
 Pneumonia
 occur between 4-12 weeks characterized by:
 distinctive repetitive
 staccato cough
 has an afebrile course with tachypnea and
 rales heard on auscultation
 Eosinophilia may be present and elevation of IgM and
IgG levels
 Radiologic findings may reveal hyperinflation
 Among older children  infection is mild atypical
pneumonia or as mycoplasma-like illness
 In adult, it appear to be associated with community-
acquired pneumonia
 May be fatal and symptomatology is indistinguishable from
other pneumonia
Diagnosis
 Tissue culture  specific diagnosis
 Fluorescent antibody test and enzyme immunoassay test
 IgM response  appear in 3 weeks, in some 3 months
trans by: Lourdes L. Lorenzo Medicine
Treatment
 Macrolides and newer Azalides  DOC
 ERYTHROMYCIN, CLARITHROMYCIN or AZITHROMYCIN
 recommended
 QUINOLONES and TETRACYCLINES avoided in children
 2 weeks duration of therapy
Trachoma
 Leading cause of PREVENTABLE BLINDNESS worldwide
 Chronic form of conjunctivitis with resulting ulceration,
scarring and opacification of cornea
 C. trachomatis (serotypes A, B, C)  most common
 Infection is also activated by presence of other bacterial
pathogens
 Transmission  direct person to person contact
Epidemiology
 Prevalent in children
 Re-infection  high in untreated cases resulting in corneal
ulceration and opacification
 Some cases of blindness follow constant trauma due to
entropion and trichiasis which are the sequelae of
conjunctival scarring and shrinking
 Self-limiting  uncomplicated cases
Treatment
 TETRACYCLINE, ERYTHROMYCIN, RIFAMPICIN and
SULFONAMIDES  useful drugs
 Hazardous to children!
 Intermittent treatment in 5 consecutive days per month
for 6 month period
 Periodic community  wide treatment = 30 days with
administration of 5days/week for 6weeks
 DOXYCYCLINE given once daily for 40 days even in children
below 9yrs of age
Prevention
 Community mass treatment and campaigns to eradicate
the disease
Genital Tract Infections
 Mostly found in sexually active adults
 Also among neonates and infants in the form of vaginitis
and urethritis acquired from birth canal
 Some infants manifest vaginitis from few weeks to several
months after a neonatal conjunctivitis and no preceding
conjunctivitis in others
 Infant with high IgM levels and serologic titers-subclinical
infection and inapparent manifestations
Treatment
 TETRACYCLINE DOC
 ERYTHROMYCIN and SULFONAMIDE alternative in INFANT
 7 day course of treatment  if uncomplicated
Page 38 of 39
LymphogranulomaVenereum
 Rare in childhood caused by:
 C. trachomatis (serotype L-1, L-2, L-3)

Transmission: direct through breaks in skin and mucous

membrane

Clinical manifestation
 Inguinal lymphadenopathy with associated systemic
disease
 Primary lesion: appear small, multiple, tender
suppuration in the genitalia extending into the inguinal
lymph nodes
 followed by fever, prostration and toxic state
especially among males
 Complication: rectal strictures and fistulous formation in
genito-urinary tract.
 Extra-genital disease: meningoencephalitis, hepatitis and
other oral and skin lesions

Diagnosis
 Clinical manifestation + history of sexual assault in children
 Tissue culture  specific test
 Serology and antigen detection-practical, available

Treatment
 SULFONAMIDES or ERYTHROMYCIN  esp. acute cases
 Clinical response is longer more than 2 weeks, such that
therapy is recommended to be given for at least 6 weeks
 POVIDONE-IODINE helpful antiseptic in lesions

Psittacosis
 Occupational disease of poultry workers and those
involve in avian species and plant processing
 C. prittaci  infective agent from discharges
 Birds and fowls  natural reservoir
Clinical Manifestation
 Respiratory tract infection with diffuse lung involvement
resulting to pneumonitis
 Some cases  systemic with “flu-like” symptoms
 Rarely  myocarditis, pericarditis, thrombophlebitis and
CNS involvement
Diagnosis
 Strong history of avian exposure and serologic titer
 Tissue culture  difficult and tedious

Treatment and Prevention

 Symptomatic: fever control and oxygenation
 TETRACYCLINE and ERYTHROMYCIN up to 10-14 days
after defervescence
 Prevention: aimed to control by treating imported birds
with TETRACYCLINE preparation

trans by: Lourdes L. Lorenzo Medicine Page 39 of 39