Review of Common Bacterial Infections in Children Part 1 PDF
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This document provides an overview of common bacterial infections in children, categorized by Gram-positive and Gram-negative types. It covers important aspects such as the etiologic agents, epidemiology, pathogenesis, clinical presentation, diagnostics, and treatment options for various conditions like pneumonia and meningitis. It also details complications associated with each infection.
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nasal packing, wound Lecture / Important Notes / Verbatim / Books infections, sinusitis, OVERVIEW: pneumonia, empyema,...
nasal packing, wound Lecture / Important Notes / Verbatim / Books infections, sinusitis, OVERVIEW: pneumonia, empyema, abscess, burns, osteomyelitis Gram Positive Infections ○ Abrupt onset Gram Negative Infections ○ High FEVER + HYPOTENSION + diffuse Reading Assignments ERYTHEMATOUS rash with GRAM POSITIVE INFECTIONS DESQUAMATION (hand and feet) ► Staphylococcus aureus during recovery (7-10days) ► Streptococcus pneumoniae ► GABHS (Streptococcus pyogenes) ► GBS (Streptococcus agalactiae ► GDS (Enterococcus) ► Diphtheria ► Listeria monocytogenes 1. Staphylococcus Aureus MOST COMMON cause of PYOGENIC INFECTION ○ pyo ~ “nana” Can cause PRIMARY or SECONDARY Bacteremia ○ Osteomyelitis, suppurative arthritis, pyomyositis, deep abscesses, pneumonia, empyema, endocarditis, pericarditis, and rarely meningitis TOXIN-MEDIATED DISEASES ○ Food poisoning, staphylococcal scarlet fever, scalded skin syndrome, and toxic shock syndrome (TSS) MOST IMPORTANT RISK FACTOR:Disruption of Intact Skin PATHOGENESIS ○ Diagnostics: BCS + Clinical ○ Tx: Oxacillin OR Vancomycin/Clindamycin ○ Remove packings or tampons + fluid replacement ○ IMPORTANT DIFFERENTIAL with SIMILAR PRESENTATION: STREPTOCOCCAL TSS (S. Diagnostics: pyogenes) ○ CS for potential focus, BCS Treatment: ○ SOURCE CONTROL Abscess I and D Removal of foreign devices ○ MSSA: Oxacillin, Co-amoxiclav ○ MRSA: Vancomycin or Clindamycin Toxic shock syndrome (TSS) ○ Menstruating women: Tampons ○ Non-menstrual TSS: 1 | Page TRANSCRIBERS: ice 2. Group A Strep (GABHS) COMPLICATIONS OF GABHS INFECTION NONSUPPURATIVE SUPPURATIVE a. Streptococcus pyogenes Acute rheumatic fever Tonsillo-pharyngeal (ARF) cellulitis or abscess Poststreptococcal Otitis media reactive arthritis Sinusitis MCC of Bacterial Pharyngitis (PSRA) Necrotizing fasciitis ○ RF and GN Scarlet fever Streptococcal Streptococcal toxic bacteremia SCARLET FEVER (2ND DISEASE) shock syndrome Meningitis/ Brain ○ URTI Acute Abscess glomerulonephritis Jugular vein ○ Rash = diffusely blanching papular Pediatric autoimmune thrombophlebitis after 1-2 days neuropsychiatric disorder associated ○ Starts in the NECK, TRUNK with group A CREASES and EXT streptococci (PANDAS) ○ Spares face ○ 3-4 days -> desquamation Diagnostics: ○ Strawberry Tongue ○ BCS ○ Impetigo ○ Throat Swab confirms GAS pharyngitis ○ ASO Titers ○ Erysipelas Treatment: ○ Perianal Dermatitis ○ Penicillin or Amoxicillin ○ Invasive disease: TSS, bacteremia, ○ Cephalosporin or Macrolides or necrotizing fasciitis Clindamycin b. Streptococcus pneumoniae Etiologic Group A Strep( S.pyogenes) Major cause of life threatening pneumoniae, Agent otitis media, bacteremia and meningitis in -GABHS children Epidemiology Occurs at all ages but is most common among Children at increased risk of IPI (Invasive school-aged children and adolescents Pneumococcal Infection) Transmission MOT: Contact with respiratory secretions RISK GROUP CONDITIONS (Droplet and Contact) Contagiousness: Acute stage of illness (not Immunocompetent Chronic Heart Disease children Chronic Lung Disease contagious after 24hrs on antibx) Diabetes mellitus Pathogenesis exotoxin (erythrogenic toxin)-mediated diffuse CSF Leaks Cochlear implants erythematous rash occurring most commonly in the setting of pharyngitis from group A Children with Sickle cell disease Streptococcus (GAS) infection functional or Congenital or acquired asplenia anatomic asplenia Clinical Linear red lines in skin folds of joints ”Pastia Presentation Children with HIV Infection Lines” immunocompromisin Chronic renal failure and nephrotic Strawberry tongue-red, mottles & peels g conditions syndrome Tender cervical nodes Chemotherapy/Radiotherapy Pharyngitis + fever CLINICAL MANIFESTATION ❖ Treatment: Amoxicillin – First Line (previously healthy, immunized children) Ampicillin/Penicillin 3rd Generation Cephalosporin (cefotaxime/ceftriaxone) Partially/unimmunized children ❖ PREVENTION Pneumococcal Vaccine PCV13 or PCV10 PPSV23 2 | Page TRANSCRIBERS: ice 3. Group B Strep 4. Corynebacterium diphtheriae - Group B Strep (Streptococcus agalactiae) DIPHTHERIA ❖ Major cause of neonatal sepsis (developed countries) ❖ Maternal vaginal or rectal colonization ❖ ❖ Diagnostics: CS (blood, urine, csf) ❖ Treatment: Penicillin G ❖ Empirical: Cefotaxime or Ampicillin PLUS Amikacin ❖ Acute contagious disease ❖ Gram (+) bacillus encapsulated; non-motile - Group D/ Enterococcus Chinese character or palisading appearance ❖ E. faecalis/E.faecium on Gram stain ❖ Hospital acquired infection ❖ ONLY RESERVOIR: HUMANS ❖ Clinical Manifestation: ASYMPTOMATIC CARRIER Sepsis, UTI, peritonitis, meningitis, TRANSMISSION endocarditis ❖ pathophysiology: localized inflammation ❖ Diagnostics: CS from rt or skin + local and systemic effects of ❖ Treatment: Penicillin G or Ampicillin PLUS potent DIPHTHERIA EXOTOXIN Amikacin ❖ Exotoxins acts on the intracellular level Resistance: Vancomycin cellular apoptosis by inactivating the elongation factor ❖ MOT:I just dropped in contact with the Case: respiratory or skin secretions ❖ 5 year-old Female ❖ incubation period: 1-5 days ❖ HPI: 3 days fever and dysphagia, with occasional cough ❖ local signs of inflammation few hours, (+) difficulty breathing, swelling of neck ❖ Immunization: BCG and Hep B ❖ Formations of Dense Necrotic coagulum (WBC, ❖ PE: awake, with stridor, (+) grayish membrane on the RBC, FIBRIN AND DEAD RESPI EPITH CELLS) tonsillopharyngeal wall, (+) swollen neck (+) tachycardia Gray brown pseudomembrane; Edematous submucosa (bleeding); Soffucation of aspirated membrane Bull next appearance; intense soft tissue edema and cervical adenitis ❖ CLINICAL MANIFESTATIONS ❖ 1. Respiratory facial and pharyngeal (most common) laryngeal and tracheobronchial malignant diphtheria extensive membranous pharyngitis plus bull neck stridor with respiratory insufficiency and death ❖ 2. Cutaneous superficial non-healing ulcer, euthymic with gray-brown membrane can’t always be differentiated with strep or staph impetigo 3 | Page TRANSCRIBERS: ice ❖ 3. systemic absorption and dissemination of the diphtheria toxin ❖ a.cardiac 5. Listeria monocytogenes myocarditis: 10-25% of cases, 2nd-3rd ❖ week of infection ❖ Major Risk for Infection: Food-Borne first sign: tachycardia Transmission disproportionate to the degree of fever ❖ Listeriosis in Pregnancy: ecg changes: st-t wave changes, qtc Higher risk of acquiring the infection prolongation and/or first degree heart due to relative impairment in block cellmediated immunity (20x higher ❖ b. neurologic than non-pregnant) 5% of mild cases and 75% in severe ❖ Neonatal Listeriosis diphtheria 2 Clinical Forms 1st few days 1. Septicemic Form (5 days of pharynx = regurgitation of swallowed life) fluids ❖ Treatment: dysphagia and nasal speech= 1st signs Ampicillin and Aminoglycoside ❖ DIPHTHERIA: LABORATORY WORKUP GRAM NEGATIVE INFECTIONS ❖ routine: cbc, throat swab membrane gs & cs specimen should be collected beneath ❖ Neisseria meningitidis the membrane including the membrane ❖ Haemophilus influenzae itself ❖ Pertussis Repeat cultures of nose & throat ❖ Pseudomonas twice(24 hours apart) after completion of treatment to ensure eradication of 1. Neiserria meningitidis organism ❖ Nasopharynx carriage ❖ Baseline ECG repeat: ECG 2x/week for 4-6 rarely enters the BS weeks ❖ Encapsulated diplococcus (detect myocarditis as early as ❖ 13 serotypes possible) A, B, C, Y, W135 ❖ DEFINITIVE DIAGNOSIS: CULTURE ❖ Aerosol droplets, direct contact with respiratory ❖ TOXIN DETECTION: ELEK TEST AND RAPID EIA secretion PCR NOT HELPFUL ❖ Clinical Manifestations ❖ DIPHTHERIA: MANAGEMENT Occult meningococcal bacteremia=rare Acute Meningococcemia 1.Neutralization of free or Diphtheria antitoxin is not READILY available loosely bound toxin with MAINSTAY OF TREATMENT FULMINANT; Diffuse Vasculitis Diphtheria antitoxin (DAT) - Fever 2.Eradication of the Pen G 100,000 units/k/day q6x 10 days or - Rash = non-blanching; organism Erythromycin 40-45mkday q6 x 14 days petechiae; purpura and 3. Management of ecchymosis Carrier state: symptom free but w/ C. diphtheria in Carriers nasopharynx - Shock; tachycardia, HPN, cold Tx: Erythromycin 40-45mkday q6x7 days extremities, CRT >3s Or Benzathine Penicillin (30kgs)1.2M units IM single dose confusion If unimmunized, complete vaccination Ff up after 2 wks & if carrier state persists, give - Disseminated Intravascular additional 10 day course of erythromycin & consider Coagulation Tosillectomy or adenoidectomy - Vasculitis (skin, heart, adrenals and mucus membrane) Meningococcal Meningitis= fever, HA, 4. Completion of Vaccination does not eliminate carriage of C. nuchal rigidity, lethargy, vomiting immunization diphtheriae in the pharynx, nose or on skin. INFECTION DOES NOT CONFER IMMUNITY Chronic Meningococcemia= rare, fever + arthritis; non-toxic appearance 5. Mgt of patient contact Household contact & Hospital contacts: -Nasopharyngeal GS & CS (weeks to months) -Eryhthromycin 40-45mkday QIDx7days or -Benzathine Penicillin (30kgs)-1.2M units IM single dose 6. Infection control STRICT ISOLATION PRECAUTION (duration of treatment i.e. 10 days) Vaccinate all EXPOSED hosp workers 4 | Page TRANSCRIBERS: ice - Diagnostic work-up - Treatment - Chemoprophylaxis - -Case definition: outbreak situation 2. Haemophilus influenzae ❖ Direct contact/extension from nasopharynx ❖ Inhalation of respiratory droplet ❖ Clinical Manifestations: Non-invasive: otitis media, sinusitis, conjunctivitis Invasive: Bacteremia, Meningitis, Sepsis Respi: Epiglottitis, pneumonia Cellulitis: preseptal and orbital Suppurative arthritis/ Osteomyelitis ❖ Diagnostics: CS ❖ Treatment: Ampicillin or Ceftriaxone 3. Bordetella pertussis ❖ PERTUSSIS ❖ Toxins: Pertussis toxin (MAJOR VIRULENCE PROTEIN) = tracheal cytotoxin 5 | Page TRANSCRIBERS: ice ❖ Exclusive pathogens of humans ❖ Natural infection or vaccination does NOT provide lifelong immunity ❖ Pertussis: classic illness Catarrhal Stage: (1-2 weeks) - Congestion, rhinorrhea, sneezing - Lacrimation, conjunctival suffusion - Low grade fever Paroxysmal Stage: (2-6 weeks) - Whooping cough (dry, intermittent, irritative hack), post-tussive vomiting - Cough evolves into paroxysms that are the HALLMARK of pertussis Convalescent Stage (weeks to months) ❖ Pertussis: infection control - Duration and severity of signs ISOLATION until 5 days after treatment and symptoms decreases initiation or 3 weeks after cough onset ❖ When to suspect? if without treatment given - For sporadic cases, a clinical case definition of Household contact cough of >14 days duration with at least 1 - Complete pertussis vaccination ASAP associated symptom of paroxysms, whoop, or - Even if vaccinated should receive post-tussive vomiting without other apparent chemoprophylaxis cause - Chemoprophylaxis same as for - Pertussis should be suspected in infants 3 weeks has ❖ Flow Chart for the Management of a Suspected elapsed since onset of cough of Pertussis Case: index case (but given for households with high risk contacts) 6 | Page TRANSCRIBERS: ice 4. Pseudomonas aeruginosa - DIAGNOSIS ❖ Classic opportunist - Presence of sulfur granules ❖ Risk Factors for Compromised host defense: - Highly suggestive of a dx of actinomycosis Trauma, neutropenia, mucositis, - Yellow, or may be white, gray or brown immunosuppression or impaired - CLINICAL MANIFESTATIONS mucociliary transport - 1. Cervicofacial Actinomycosis - Mass ❖ High colonization rate at 50-70% in the neck or submandibular region Prolonged hospitalization weeks to months) Use of broad spectrum antibiotics - 2. Abdominal and Pelvic Actinomycosis- Chemotherapy Delayed diagnosis is most typical in Mechanical ventilation this manifestation; Disruption of Urinary catheter mucosa of the GI tract ❖ Pathogenesis: - 3. Thoracic Actinomycosis - May Adherence of pili to epithelium manifest as an endobronchial infection, previously damaged by injury or a tumor-like lesion, diffuse pneumonia, infection or pleural effusion Exotoxin A: local necrosis and - 4. Cerebral and Other Forms of facilitates systemic bacterial infection Actinomycosis- CNS involvement is Biofilm formation chronic persistence often the result of hematogenous Clinical Manifestation: spread to the brain parenchyma from a Opportunistic infection in distant site but can also result from immunocompromised hosts Ecthyma contiguous spread from a cervicofacial gangrenosum lesion Pink macules hemorrhagic nodules - TREATMENT ulcers, ecchymotic and gangrenous - Prompt initiation of antibiotics is important to centers eschar formation resolve the infection ❖ TREATMENT - Most Actinomyces spp. Are - 3rd generation Cephalosporin susceptible to penicillin G (drug of - 4th generation Cephalosporin choice) - Broad spectrum antibiotics - ❖ Nocardia READING ASSIGNMENT - Primarily opportunistic pathogens infecting 44 immunocompromised persons ❖ Actinomyces - Weakly acid fast - Anaerobic or microaerophilic, nonsporulating, - Nocardiosis nonmotile gram-positive bacteria Acute, subacute, or chronic - Actinomycosis suppurative - Often presents as an indolent granulomatous, - infections with a tendency for remissions and suppurative process with potential for direct exacerbations extension to contiguous tissue across natural - PATHOGENESIS anatomic barriers and formation of draining Environmental saprophytes that are fistulas and sinus tracts ubiquitous in soil and decaying - Endogenous flora: oropharynx, GI tract or vegetable matter and have been urogenital tract isolated from soil - A. israelii: predominant spp causing human can disseminate from primary site of actinomycosis infection to any organ or - "great imitator" that mimics: musculoskeletal location - Appendicitis,pseudoappendicitis, amoebiasis, CNS: most concerning and most malignancy, and IBD common secondary site of infection - PATHOGENESIS ❖ CLINICAL AND RADIOGRAPHIC - 3 most common sites in order of frequency: MANIFESTATIONS - 1. Cervicofacial Clinical presentation can be nonspecific - 2. Abdominal and pelvic o Fever (60%) - 3. Thoracic regions o Cough (30%) - Hallmark: contiguous spread that fails to o Dyspnea (25%) respect tissue or fascial planes - Neurologic complaints: - Dense cellular infiltrates and suppuration that o Headache, confusion or form many interconnecting abscesses and altered mental status sinus tracts o Weakness, speech impairment - Sporotrichoid nocardiosis 7 | Page TRANSCRIBERS: ice o “superficial ulcers” - - Predisposing factors: o Skin infection congenital cardiac - Mycetoma malformations or rheumatic - → Chronic, progressive valvular disease infection developing days to ❖ DIAGNOSIS months after inoculation, - Isolation of bacteria or by a positive NAAT from usually on a distal location on blood, synovial fluid, or bone tissue the limbs ❖ TREATMENT - Cavitary lesions: more common in - K. kingae is usually highly susceptible to patients with an underlying penicillin and cephalosporins but exhibits immunocompromising condition decreased susceptibility to oxacillin ❖ DIAGNOSIS - Routine blood culture (25% of patients) - Bronchoscopy, tissue biopsy or abscess ❖ CHANCROID aspiration Haemophilus ducreyi ❖ TREATMENT → Fastidious gram (-) bacilli - Trimethoprim-sulfamethoxazole - Sexually transmitted disease → Sulfonamide formulation that is - Painful genital ulceration and inguinal recommended lymphadenopathy - Sulfadiazine, Sulfisoxazol - Risk factor for transmission of HIV - Surgical drainage of abscess ❖ CLINICAL MANIFESTATIONS - → Helpful in hastening resolution of - Incubation period: 4-7 days Nocardiosis - → Small, inflammatory papule on preputial orifice or frenulum in men and on the labia, fourchette, or ❖ KINGELLA KINGAE perianal region in women - Most common etiology of septic arthritis, - Pustular, eroded, and ulcerative within 2-3 osteomyelitis, and spondylodiscitis in young days children - Lymphadenopathy can become fluctuant to ❖ PATHOGENESIS form buboes, which can spontaneously rupture - Repeats-in-Toxin (RTX) - Complications: - → Exhibits deleterious activity to - → Phimosis in men and secondary respiratory epithelial cells bacterial infection macrophages, and synoviocytes ❖ DIAGNOSIS - May play a role in disrupting the - Clinical presentation and exclusion of both respiratory mucosa, promoting survival syphilis and HSV infection of the bacterium in the bloodstream, - Gram stain of ulcer secretions: “school of fish” and facilitate invasion of skeletal - Culture: sensitivity of 80% system tissues - Infants and children: strong evidence of sexual ❖ CLINICAL DISEASE abuse - Septic arthritis: most common invasive K. ❖ TREATMENT kingae infection in children Most H. ducreyi are resistant to - Followed by: bacteremia, osteomyelitis, and penicillin and ampicillin endocarditis - Treatment recommendation= - 1. Septic arthritis - → Azithromycin (1g as a single dose - 2. Osteomyelitis orally) - - Involves long bones of - → Ceftriaxone (250 mg as a single extremities dose IM) - - Also calcaneus, talus, - Alternative: sternum, and clavicle - → Erythromycin (500 mg 3x daily PO - 3. Spondylodiscitis for 7d) - Involves lumbar invertebral - → Ciprofloxacin (500 mg 2x daily PO spaces, thoracolumbar, for 3d,≥18 yrs old) thoracic, lumbosacral, cervical ❖ MORAXELLA CATARRHALIS disks - Unencapsulated gram-negative diplococcus - Limping, lumbar pain, back - Human-specific pathogen that colonize stiffness, refusal to sit or walk, respiratory tract beginning in infancy neurologic symptoms - Otitis media – most impt CM of the organism - 4. Occult Bacteremia - Age – most impt determinant of prevalence of - 5. Endocarditis upper respiratory tract colonization 8 | Page TRANSCRIBERS: ice - PATHOGENESIS - Aeromonas diarrhea: watery and - Complement-resistant strains – more self-limited strongly assoc. with virulence - - Dysentery-like syndrome with - Adhesins – its presence reflects the blood and mucus importance of adherence to respiratory - - Fever, abdominal pain, epithelial surface in the pathogenesis vomiting of infection ❖ 2. Skin and Soft Tissue Infections - Biofilms – encased in a matrix → 2nd most common presentation of attached to a surface Aeromonas - → More resistant to antibiotics → Predisposing factors: - CLINICAL MANIFESTATIONS o Local trauma and exposure to - Migration – mechanism of infection contaminated fresh water - 1. Acute Otitis Media → Reported following bites from animal - - Most common reason that spp: alligators, tigers, bears, snakes, children receive antibiotics tick bites - Predominant causes: Aeromonas cellulitis: most common o S. pneumonia skin manifestation o H. influenza o Presents similar to other forms of o M. catarrhalis bacterial cellulitis (milder) ❖ 3. Septicimia - 2. Recurrent Otitis Media with Effusion 3rd most common presentation of - - Presence of fluid in the infection middle ear in the absence of → Fever and GI symptoms (abdominal s/s of acute infection pain, nausea, vomiting, and diarrhea - Otitis prone - Children who → Ecthyma gangrenosum-like lesions experience 4 or more episodes (2-4%) of acute otitis media in a year ❖ Other infections or who have at least 8 mo of ❖ GI infections middle ear effusion in a year - Necrotizing gastroenteritis - 3. Sinusitis - Peritonitis - Cholecystitis - 4. Bacteremia - Appendicitis - DIAGNOSIS - Liver and pancreas abscess formation ❖ Pneumatic otoscopy – demonstration of fluid in ❖ Pulmonary infections middle ear (otitis media) - Tracheobronchitis ❖ Tympanocentesis – not routinely performed - Pneumonia ❖ Sinus puncture - Empyema - Lung abscess formation ❖ Cardiovascular infections - Endocarditis ❖ AEROMONAS AND PLESIOMONAS - Septic embolism ❖ Aeromonas ❖ Musculoskeletal infections - 2 major group of isolates: - Osteomyelitis - 1. Nonmotile psychrophilic organisms - Pyogenic arthritis - Pyomyositis (infect cold-blooded animals) - Necrotizing fasciitis - 2. Motile mesophilic organisms (infect ❖ DIAGNOSIS & TREATMENT DIAGNOSIS & humans and other warm-blooded TREATMENT animals) Culture - Aeromonas cytotoxic enterotoxin Aeromonas enteritis is usually (Act/aerolysin) self-limited → Lyse erythrocytes, inhibit Antimicrobial therapy: to consider in phagocytosis, and induce cytotoxicity px with protracted diarrhea, in eukaryotic cell dysentery-like illness, or underlying ❖ CLINICAL MANIFESTATIONS conditions (hepatobiliary dse or ❖ 1. Enteritis immunocompromised state - → Most common clinical manifestation of Septicimia infection with Aeromonas o 4th generation cephalosporin - → Occurs primarily among children