micro notes
TRANSCRIPT
Microbiology
Gram-positives
Cocci
Streptococcus
Streptococcus pyogenes
Streptococcus agalactiae
Viridans group Streptococcus
Streptococcus pneumoniae
Enterococcus
Enterococcus faecalis
Enterococcus faecium
Staphylococcus
Staphylococcus aureus
Staphylococcus epidermidis
Staphylococcus saprophyticus
Pepto-streptococcus
Rods
Spore-forming
Bacillus
Bacillus cereus
Bacillus anthracis
Clostridium
Clostidium botulinum
Clostridium tetani
Clostridium perfringens
Clostridium difficile
Clostridium septicum
Non-spore-forming
Listeria monocytogenes
Corynebacterium diphteriae
Pleomorphs
Actinomyces
Nocardia
Obligate aerobeAerobeMicroaerophilicFacultative anaerobeAnaerobe
Gram-Positive Bacteria
Gram-negatives
Cocci
Neisseria
Neisseria meningitidis Neisseria gonorrhoeae
Rods
(see next page)
Obligate intracellulars
Rickettsia Bartonella Chlamydia
Chlamydia trachomatis
Chlamydia pneumoniae Chlamydia psittaci
Spirochetes
Treponema pallidum
Borellia
Leptospira
Obligate aerobeAerobeMicroaerophilicFacultative anaerobeAnaerobe
Gram-Negative Bacteria
Gram-negative rods
Enterobacteriaceae
(See next page)
Bacteroidaceae
Bacteroides fragilis
Vibrionaceae
Vibrio cholera
Vibrio parahaemolyticus
Vibrio vulnificus
Campylobacterales
Campylobacter
Helicobacter pylori
Non-fermenters
Oxidase-positive
Pseudomonas aeruginosa
Burkholderia cepacia complex
Burkholderia pseudomallei
Oxidase-negative
Acinetobacter baumanii
Stenotromonas maltophilia
Fastidious GNRs
Bordatella pertussis
Legionella pneumophila
Haemophilus
Haemophilus influenzae
Haemophilus parainfluenzae
Haemophilus ducreyi
Obligate aerobeAerobeMicroaerophilicFacultative anaerobeAnaerobe
Gram-Negative Rods
Enterobacteriaceae
Aeromonas* Escherichia coli Salmonella Shigella Klebsiella
Klebsiella granulomatosis
Klebsiella pneumoniae
Proteus
Proteus vulgaris
Proteus mirabilis
Yersinia
Yersinia enterocolitica
Yersinia pseudotuberculos
is
Yersinia pestis
Opportunistic pathogens
Enterobacter Serratia
Citrobacter
Obligate aerobeAerobeMicroaerophilicFacultative anaerobeAnaerobe
Enterobacteriaceae
Atypicals
Mycobacteria
Mycobacterium tuberculosis
Mycobacterium leprae
Non-tuberculoid Mycobacteria
Slow-growers
Mycobacterium avium complex
Mycobacterium kansasii
Mycobacterium marinum
Mycobacterium ulcerans
Fast-growers
Mycobacterium abscessus
Mycobacterium chelonae
Mycobacterium fortuitum
Mycoplasma
Mycoplasma genitalium
Mycoplasma pneumoniae
Obligate aerobeAerobeMicroaerophilicFacultative anaerobeAnaerobe
Atypical Bacteria
Streptococcus pyogenesCharacteristics– Gram-positive cocci in chains– Catalase-negative– Oxidase-negative– Beta-hemolytic– Lancefield antigen A– Normal oropharyngeal flora
Virulence Factors Pathogenesis Clinical Findings
Capsule factorsHyaluronic acid – immune evasion
Cell wall factorsM protein – adhesion, immune evasionC polysaccharide – Lancefield antigens,
not virulent
ExotoxinsPyrogenic exotoxins (A, B, C) –
superantigens produced by some strains
Streptolysin – hemolyticStreptokinase, hyaluronidase,
endonucleases, proteases – tissue destruction
Local invasion and release of exotoxins
Ab-mediated post-infection sequelae
PharyngitisSkin infections
FolliculitisCellulitisImpetigoNecrotizing fasciitis
Scarlet feverToxic shock syndrome
Rheumatic feverHeart – myocarditis and endocarditisJoints – arthralgia and arthritisSkin - erythema marginatumCNS – chorea
Acute glomerulonephritis
Diagnosis– Gram stain (GPC in chains)– Culture (beta-hemolytic ,sensitive to bacitracin)– RADT for pharyngitis
Treatment– Penicillin G or penicillin V– Erythromycin– Oxacillin
Streptococcus agalactiaeCharacteristics– Gram-positive cocci in chains– Catalase-negative– Oxidase-negative– Beta-hemolytic– Lancefield antigen B– Normal vaginal flora
Virulence Factors Pathogenesis Clinical Findings
Capsule factors – immune evasion
Cell wall factorsC polysaccharide – Lancefield antigens,
not virulent
ExotoxinsStreptolysin – hemolyticStreptokinase, hyaluronidase,
endonucleases, proteases – tissue destruction
Infection in newborns during birth
Can also cause disease in elderly, diabetics, and the immunocompromised
Neonatal septicemiaNeonatal meningitisNeonatal pneumonia
Early onset (first 6 days) – mostly septicemia, but meningitis and pneumonia possible
Late onset (up to 3 months) – severe meningitis and septic shock possible
Diagnosis– Urine Gram stain (GPC in chains)– Urine culture (beta-hemolytic)
Treatment– Penicillin G
Viridans group StreptococcusCharacteristics– Gram-positive cocci in chains– Catalase-negative– Oxidase-negative– Alpha-hemolytic– No Lancefield antigens– Normal oral and GI flora
Virulence Factors Pathogenesis Clinical Findings
Capsule factors – immune evasion
ExotoxinsStreptolysin – hemolyticStreptokinase, hyaluronidase,
endonucleases, proteases – tissue destruction
Dental work can lead to transient bacteremia and infection
Dental caresSubacute endocarditisLiver and brain abscesses
Septicemia – in immunocompromised individuals
Diagnosis– Gram stain (GPC in chains)– Culture (alpha-hemolytic, resistant to optochin)
Treatment– Penicillin G
Streptococcus pneumoniaeCharacteristics– Gram-positive cocci in pairs– Catalase-negative– Oxidase-negative– Alpha-hemolytic– No Lancefield antigens– Normal respiratory flora
Virulence Factors Pathogenesis Clinical Findings
Capsule factors – immune evasion
Cell wall factorsSurface protein A (PspA) – immune
evasion
ExotoxinsStreptolysin – hemolyticStreptokinase, hyaluronidase,
endonucleases, proteases – tissue destruction
Autolysin – kills bacteria, releases pneumolysin
Pneumolysin – cytolytic, pro-inflammatory
Infections following a respiratory virus or due to oropharyngeal aspiration (patients with altered conciousness)
Lobar pneumoniaMeningitisSinusitisOtitis media
Diagnosis– Gram stain (GPC in pairs)– Culture (alpha-hemolytic, sensitive to optochin)– Quellung reaction
Treatment– Penicillin G– Erythromycin– Ceftriaxone
Enterococcus faecalisCharacteristics– Gram-positive cocci in chains– Catalase-negative– Oxidase-negative– Normal GI flora, more prevalent than
Enterococcus faecium
Virulence Factors Pathogenesis Clinical Findings
Capsule factors – immune evasion
ExotoxinsHyaluronidase, endonucleases,
proteases – tissue destruction
UTIsSubacute endocarditisCholecystitis
Septicemia – in immunocompromised individuals
Diagnosis– Gram stain (GPC in pairs)– Culture
Treatment– Ampicillin (possibly with gentamicin)
Enterococcus faeciumCharacteristics– Gram-positive cocci in chains– Catalase-negative– Oxidase-negative– Normal GI flora, less prevalent than
Enterococcus faecium, but notable for the development of vancomycin resistance
Virulence Factors Pathogenesis Clinical Findings
Capsule factors – immune evasion
ExotoxinsHyaluronidase, endonucleases,
proteases – tissue destruction
UTIsSubacute endocarditisCholecystitis
Septicemia – in immunocompromised individuals
Diagnosis– Gram stain (GPC in pairs)– Culture
Treatment– Ampicillin (possibly with gentamicin)– Linezolid (for VRE)
Staphylococcus aureusCharacteristics– Gram-positive cocci in clusters– Catalase-positive– Oxidase-negative– Beta-hemolytic– Normal skin, GI, and vaginal flora
Virulence Factors Pathogenesis Clinical Findings
Capsule factors – immune evasion
Cell wall factorsSurface protein A (SpA) – immune
evasion
ExotoxinsStaphylokinase, hyaluronidase,
endonucleases, proteases – tissue destruction
Hemolysins and leukocidins – hemolytic
Coagulase – bind prothrombin to form pro-clotting factor staphylothrombin
Clumping factors (A,B) – promote clotting
SuperantigensEnterotoxins (A-D) – food poisoningExfoliatins (A,B) – scalded skin
syndromeToxic shock syndrome toxin (TSST) –
toxic shock syndrome
Invasion and exotoxin release
Superantigen-mediated
PneumoniaSkin infections
ImpetigoCellulitisCutaneous abscessesWound infections
MeningitisOsteomyelitis – in childrenAcute endocarditisSeptic arthritisUTIsSepticemia
Toxic shock syndromeGastroenteritis (food poisoning)Scalded skin syndromeNecrotizing fasciitis
Diagnosis– Gram stain (GPC in clusters)– Culture (beta-hemolytic, golden yellow colonies)
Treatment– Oxacillin– Vancomycin (for MRSA)– Clindamycin
Staphylococcus epidermidisCharacteristics– Gram-positive cocci in clusters– Catalase-positive– Oxidase-negative– Gamma-hemolytic– Normal skin flora
Virulence Factors Pathogenesis Clinical Findings
Capsule factorsBiofilms – adherence and immune
evasion
Opportunistic infections, biofilms can adhere to prosthetics
Prosthetic infectionsArtificial jointsArtificial heart valves
Sepsis - from IV linesUTIs
Septicemia – in neonates and immunocompromised individuals
Diagnosis– Gram stain (GPC in pairs)– Culture (gamma-hemolytic, novobiocin sensitive)
Treatment– Vancomycin
Staphylococcus saprophyticusCharacteristics– Gram-positive cocci in clusters– Catalase-positive– Oxidase-negative– Gamma-hemolytic– Normal skin flora
Virulence Factors Pathogenesis Clinical Findings
Capsule factorsBiofilms – adherence and immune
evasion
UTIs – in sexually active young women
Diagnosis– Gram stain (GPC in pairs)– Culture (gamma-hemolytic, novobiocin resistant)
Treatment– Vancomycin
Bacillus anthracisCharacteristics– Gram-positive rods– Catalase-positive– Oxidase-negative– Gamma-hemolytic– Non-motile– Spore-forming– Facultatively intracellular– Zoonotic and potentially food-borne
Virulence Factors Pathogenesis Clinical Findings
Capsule factors – immune evasion
ExotoxinsProtective antigen (PA) – promotes
endocytosisEdema factor (EF) – binds PA to form
edema toxin, stimulates cAMP and edema
Lethal factor (LF) – binds PA to form lethal toxin, kills macrophages
Spores can enter via the skin, lungs, or GI; germinate in macrophages and spread via RES
Cutaneous anthraxPruritic papule -> bulbous lesion ->
necrotic ulcer -> black escharEdema and lymphadenopathy
Inhalation anthraxMediastinal hemorrhageAngina, dyspnea, cyanosis, and shock
Gastrointestinal anthraxUlcersRegional lymphadenopathyNausea, vomiting, bloody diarrhea,
and sepsis
Diagnosis– CSF, blood, or pleural Gram stain (GPRs)– CSF, blood, or pleural culture
Treatment– Amoxicillin– Doxycycline– Ciprofloxacin
Bacillus cereusCharacteristics– Gram-positive rods– Catalase-positive– Oxidase-negative– Beta-hemolytic– Motile– Spore-forming– Facultatively intracellular– Environmental and food-borne
Virulence Factors Pathogenesis Clinical Findings
Heat-labile toxin – stimulates cAMP and fluid/electolyte secretion
Heat-stabile toxin – stimulates cGMP and fluid/electrolyte secretion
Spores can germinate in GI and produce toxins
Infection following penetrating trauma
Foodborne illnessDiarrheal – due to heat labile-toxinEmetic – due to heat stabile-toxin
Ocular diseaseWound infections
Immunocompromised individuals – endocarditis, abscesses, and bacteremia
Diagnosis– Gram stain (GPRs) of suspected food source– Culture (beta-hemolytic, large, feathery colonies)
of suspected food sourceTreatment– Amoxicillin– Doxycycline– Ciprofloxacin
Clostridium perfringensCharacteristics– Gram-positive rods– Non-motile– Spore-forming– Environmental , normal GI flora
Virulence Factors Pathogenesis Clinical Findings
Alpha toxin – cytotoxicBeta toxin – associated with necrotizing
enterocolitisEnterotoxin – associated with diarrheal
symptoms
Inoculation with spores which germinate
CellulitisWound infectionsClostridial myonecrosis (gas gangrene)Necrotizing enterocolitis
Diagnosis– Gram stain – Anaerobic culture
Treatment– Surgical debridement– Penicillin G and clindamycin
Clostridium difficileCharacteristics– Gram-positive rods– Motile– Spore-forming– Environmental , normal GI flora
Virulence Factors Pathogenesis Clinical Findings
Toxin A– enterotoxin (diarrheal)Toxin B – cytotoxinH antigen (flagellar) – flagellar proteins
Pathogenic overgrowth following antibiotic therapy
Pseudomembranous colitisAntibiotic-associated diarrhea
Diagnosis– Immunoassay or PCR to detect toxin in stool
Treatment– Withdrawal of previous antibiotic– Metronidazole– Vancomycin (orally)
Clostridium botulinumCharacteristics– Gram-positive rods– Motile– Spore-forming– Environmental, infections acquired
through improper canning (adults), fresh honey (infants)
Virulence Factors Pathogenesis Clinical Findings
Toxin A-G – released on bacterial deathNeurotoxin – H antigen (flagellar) – flagellar proteins
Ingestion of/inoculation with spores which germinate
Foodborne botulismEarly nausea, vomiting, diarrheaCranial nerve palsies Descending flaccid paralysisRespiratory paralysis
Infant botulismConstipationFlaccid paralysis
Wound botulismCranial nerve palsies Descending flaccid paralysisRespiratory paralysis
Diagnosis– Detection of stool in mouse bioassay
Treatment– Surgical debridement– Equine serum (for adults)– Human botulism IgG (for infants)
Clostridium tetaniCharacteristics– Gram-positive rods– Motile– Spore-forming– Environmental
Virulence Factors Pathogenesis Clinical Findings
Tetanospasmin – blocks inhibitory neurotransmitters, prolonging muscle spasms
H antigen (flagellar) – flagellar proteins
Inoculation with spores which germinate and travel to peripheral motor neuron plates and release exotoxin
Tetanus“Lockjaw”Risus sardonicusArched back
Diagnosis– Gram stain– Anaerobic culture
Treatment– Supportive care– Human tetanus Immunoglobulin– Metronidazole– Vaccine
Clostridium septicumCharacteristics– Gram-positive rods– Motile– Spore-forming
Virulence Factors Pathogenesis Clinical Findings
Alpha toxin – cytotoxicH antigen (flagellar) – flagellar proteins
Mechanism unknown, may be invasive
Gas gangreneColorectal cancer
Diagnosis– Gram stain– Anaerobic culture
Treatment– Penicillin G– Surgical debridement
Bacteroides fragilisCharacteristics– Gram-negative rods– Motile– Normal GI flora
Virulence Factors Pathogenesis Clinical Findings
Capsule – no LPS, but causes abscess formation
Perforation of GI (surgery or trauma) allows B. fragilis to enter the peritoneum, where it can cause abscesesAlso possible following a primary bacterial infection (i.e. appendicitis)
Abscessses – GI, pelvis, lungs
Diagnosis– Gram stain– Anaerobic culture
Treatment– Metronidazole– Clindamycin– Surgical drainage of abscesses
Listeria monocytogenesCharacteristics– Gram-positive rods– Catalase-positive– Oxidase-negative– Beta-hemolytic– Motile– Facultatively intracellular– Environmental and food-borne
Virulence Factors Pathogenesis Clinical Findings
Internalin A – promotes phagocytosisListeriolysin O – facilitates escape from
phagosomeAct A – induces actin polymerization to
spread to other cells
Capable of crossing GI mucosa by inducing endocytosis; hematogenous spread and capable of surviving in macrophages in immunodeficient individuals
Immunocompetent individualsDiarrheaFever and chillsPain – abdominal, headache, myalgia
Pregnant womenMostly asymptomaticGastroenteritisBacteremiaStillbirth
NeonatesGranulomatous infantisepticum –
granulomatous inflammation and splenomegaly
Early-onset (first week) – sepsis, bacteremia
Late-onset (within 2 weeks) – meningitis
Immunocompromised individuals
BacteremiaMeningitis
Diagnosis– CSF Gram stain (GPRs)– CSF culture
Treatment– Ampicllin– Trimethoprim and sulfamethoxazole
Corynebacterium diphtheriaeCharacteristics– Pleiomorphic/club-shaped Gram-positive
rods– Catalase-positive– Oxidase-negative– Beta-hemolytic– Non-motile– Strictly pathogenic
Virulence Factors Pathogenesis Clinical Findings
Exotoxin – cytotoxic Spread via respiratory droplets, forms pharyngeal pseudomembrane and secretes exotoxin (non-invasive) affecting heart and nervous system
Cutaneous infection also possible
Respiratory infectionFever, malaise, sore throatPharyngeal pseudomembrane“Bull’s neck” – distortion of lower
airway
MyocarditisNeurological symptoms
Cutaneous diphtheria – non-healing ulcers, dirty gray membrane
Diagnosis– Gram stain (GPRs) of pseudomembrane– Culture on selective media (tellurite or Tinsdale)
Treatment– Diphtheria antitoxin– Penicillin– Erythromycin– Vaccination
ActinomycesCharacteristics– Pleiomorphic Gram-positive rods– Normal oral and GI flora
Virulence Factors Pathogenesis Clinical Findings
Indolent infection leading to erosive abscesses and “sulfur granules”
Cervicofacial actinomycosisThoracic actinomycosisAbdominal acitnomycosis
Diagnosis– Presence of “sulfur granules”– Anaerobic culture (“molar tooth” colonies,
branching chains or beaded filaments)Treatment– Penicillin G– Surgical removal of abscesses
NocardiaCharacteristics– Pleiomorphic Gram-positive rods– Weakly acid-fast– Strictly pathogenic, environmental,
respiratory transmission, immunocompromised patients at risk
Virulence Factors Pathogenesis Clinical Findings
Slow-growing Cutaneous nocardiosisCellulitisAbscesses – lung, kidneys, CNSMycetoma – chronic osteomyelitis in
feet caused by N. brasiliensis
Pulmonary and disseminated nocardiosis – in immunodeficient
Pneumonia with nodular and cavitary infiltrates
Dissemination to brain
Diagnosis– Gram stain or acid-fast stain– Culture (branching chains or beaded filaments)
Treatment– Trimethoprim and sulfamethoxazole
EnterobacterCharacteristics– Gram-negative rods– Indole-negative– Lactose-fermenter– Motile– Normal GI flora, can cause opportunistic
infections
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSK antigen (capsular) – capsular
polysaccharideH antigen (flagellar) – flagellar proteinsPili – promote colonization
Nosocomial infections
Diagnosis– Gram stain (GPRs)– Culture on MacConkey agar
Treatment– Cefepime
CitrobacterCharacteristics– Gram-negative rods– Indole-positive– Lactose-fermenter– Motile– Normal GI flora, can cause opportunistic
infections
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSK antigen (capsular) – capsular
polysaccharideH antigen (flagellar) – flagellar proteinsPili – promote colonization
Neonatal meningitisSepsis
Diagnosis– Gram stain (GPRs)– Culture on MacConkey agar
Treatment– Ceftriaxone
SerratiaCharacteristics– Gram-negative rods– Indole-positive– Non-lactose fermenter– Motile– Normal GI flora, can cause opportunistic
infections
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSK antigen (capsular) – capsular
polysaccharideH antigen (flagellar) – flagellar proteinsPili – promote colonization
PneumoniaUTIsSepsis
Diagnosis– Gram stain (GPRs)– Culture on MacConkey agar
Treatment– Levaquin– Ceftriaxone
Escherichia coliCharacteristics– Gram-negative rods– Beta-hemolytic– Indole-positive– Lactose-fermenter– Motile– Normal GI flora, but can acquire
virulence factors
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSK antigen (capsular) – capsular
polysaccharideH antigen (flagellar) – flagellar proteinsPili – promote colonizationHeat-labile toxin (LT) – stimulates cAMP
and fluid/electolyte secretionHeat-stabile toxin (ST) – stimulates cGMP
and fluid/electrolyte secretionShiga-like toxin (I,II) – bind to epithelial
cells and damage them
Enterotoxigenic (ETEC) – produce LT and ST
Enteroinvasive (EIEC) – invasive
Shiga toxin producing (STEC/EHEC) – produces Shiga-like toxin
Enteropathogenic (EPEC)Enteroaggregative (EAEC)Diffusely aggregative
(DAEC)
Diarrheagenic intestinal infectionsTraveler’s diarrhea – ETECBloody diarrhea – EIEC, STECHemorrhagic colitis – STECHemolytic uremic syndrome – STEC
Intra-abdominal infectionsPeritonitisLiver abscessesCholecystitis
UTIsMeningitis – in neonatesPneumonia – hospital-acquiredSepsis
Diagnosis– Gram stain (GPRs)– Culture on MacConkey agar
Treatment– Fluids (intestinal infections)– Anitibiotics for other infections
– Cephalosporins– Amingoglycosides– Trimethoprim and sulfamethoxazole– Fluoroquinolones
Klebsiella pneumoniaeCharacteristics– Gram-negative rods– Gamma-hemolytic– Indole-negative– Lactose-fermenter– Non-motile– Environmental, normal skin and GI flora,
common nosocomial infection, causes infection in alcoholics and diabetics
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSK antigen (capsular) – capsular
polysaccharidePili – promote colonization
Necrotic cavitary pneumoniaUTIsSepsis
Diagnosis– Gram stain (GPRs)– Culture on MacConkey agar
Treatment– Ceftriaxone– Ciprofloxacin
Klebsiella granulomatosisCharacteristics– Gram-negative rods– Gamma-hemolytic– Indole-negative– Lactose-fermenter– Non-motile– Sexually transmitted– Endemic in Southeast Asia and Africa
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSK antigen (capsular) – capsular
polysaccharidePili – promote colonization
Granuloma inguinale (donovanosis)Painless ulcerative lesion
Diagnosis– Tissue biopsy
Treatment– Doxycycline
Proteus mirabilisCharacteristics– Gram-negative rods– Gamma-hemolytic– Indole-negative– Non-lactose fermenter– Highly motile– Environmental, common nosocomial
infection
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSK antigen (capsular) – capsular
polysaccharideH antigen (flagellar) – flagellar proteinsPili – promote colonizationUrease – alkalinizes urine, leading to
kidney/bladder stones
UTIsUrolithiasisSepsis
Diagnosis– Gram stain (GPRs)– Swarming colonies on MacConckey agar culture
Treatment– Ampicillin– Ceftriaxone
Proteus vulgarisCharacteristics– Gram-negative rods– Gamma-hemolytic– Indole-posiive– Non-lactose fermenter– Highly motile– Environmental, common nosocomial
infection, usually seen in immunocompromised individuals
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSK antigen (capsular) – capsular
polysaccharideH antigen (flagellar) – flagellar proteinsPili – promote colonizationUrease – alkalinizes urine, leading to
kidney/bladder stones
UTIsUrolithiasisSepsis
Diagnosis– Gram stain (GPRs)– Swarming colonies on MacConckey agar culture
Treatment– Ampicillin– Ceftriaxone
ShigellaCharacteristics– Gram-negative rods– Gamma-hemolytic– Indole-posiive– Non-lactose fermenter– Non-motile– Strictly pathogenic, fecal-oral and
person-to-person transmission, can cause nursing home and daycare outbreaks
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSK antigen (capsular) – capsular
polysaccharidePili – promote colonizationShiga toxin (I, II) – bind to epithelial cells
and damage them
Capable of invading GI mucosa (via endocytosis and escape) and releasing exotoxin
Bacillary dysnteryFeverAbdominal crampsTenesmusBloody diarrhea
Diagnosis– Stool Gram stain (GPRs)– Stool culture on MacConckey agar
Treatment– Ampicillin– Trimethoprim and sulfamethoxazole– Ciprofloxacin
SalmonellaCharacteristics– Gram-negative rods– Gamma-hemolytic– Indole-posiive– Non-lactose fermenter– Motile– Strictly pathogenic, acquired from animal
feces (except Salmonella typhi)
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSVi antigen – capsular protein, like K
antigenH antigen (flagellar) – flagellar proteins
Capable of invading GI mucosa (via pinocytosis and escape) and lamina propria, hematogenous spread
S. typhi is facultatively intracellular in macrophages, leading to systemic infection, bacteria can lie dormant in gallbladder for years
GastroenteritisNausea, vomiting, crampsWatery diarrhea
Typhoid feverFeverAbdominal painHepatosplenomegalyRose spotsSepsis
Diagnosis– Stool Gram stain (GPRs)– Stool culture on MacConckey agar
Treatment– Fluids– Antibiotics for typhoid fever
– Ampicillin– Trimethoprim and sulfamethoxazole– Ciprofloxacin
Yersinia enterocoliticaCharacteristics– Gram-negative rods– Gamma-hemolytic– Non-lactose fermenter– Motile– Strictly pathogenic, acquired from animal
feces, undercooked pork, blood transfusions
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSK antigen – capsular proteinH antigen (flagellar) – flagellar proteinsHeat-stabile toxin (ST) – stimulates cGMP
and fluid/electrolyte secretion
Invasive infection Acute enterocolitisIleal ulcers
Diagnosis– Stool Gram stain (GPRs)– Stool culture on MacConckey agar
Treatment– Fluids
Yersinia pseudotuberculosisCharacteristics– Gram-negative rods– Gamma-hemolytic– Non-lactose fermenter– Motile– Strictly pathogenic, acquired from animal
feces
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSK antigen – capsular proteinH antigen (flagellar) – flagellar proteins
Invasive infection “Pseudo-appendicitis”FeverRight lower quadrant pain
Diagnosis– Stool Gram stain (GPRs)– Stool culture on MacConckey agar
Treatment– Fluids
AeromonasCharacteristics– Gram-negative rods– Oxidase-positive– Motile– Environmental, associated with aquarium
water
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSVi antigen – capsular protein, like K
antigenH antigen (flagellar) – flagellar proteinsHeat-stabile toxin (ST) – stimulates cGMP
and fluid/electrolyte secretion
GastroenteritisWound infectionsHemolytic uremic syndrome (rare)Sepsis
Diagnosis– Stool Gram stain (GPRs)– Stool culture on MacConckey agar
Treatment– Fluids
CampylobacterCharacteristics– Gram-negative rods– Oxidase-positive– Motile– Strictly pathogenic, present in
undercooked poultry and milk
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSK antigen (capsular) – capsular
polysaccharideH antigen (flagellar) – single polar
flagellumEnterotoxin – stimulates cAMP and
fluid/electolyte secretion
Invasive infection Bloody diarrhea
Guillan-Barre – potential sequela
Diagnosis– Stool Gram stain (comma-shaped rods with single
polar flagellum)– Stool culture on MacConckey agar
Treatment– Fluoroquinolone– Erythromycin
Helicobacter pyloriCharacteristics– Gram-negative rods– Oxidase-positive– Motile– Normal GI flora
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSK antigen (capsular) – capsular
polysaccharideH antigen (flagellar) –polar flagella
Duodenal ulcersChronic gastritis
Diagnosis– Stool Gram stain (comma-shaped rods with tuft of
polar flagella)– Stool culture on MacConckey agar
Treatment– Bismuth with antibiotics (ampicillin,
metronidazole, or tetracycline)
Vibrio choleraeCharacteristics– Gram-negative rods– Oxidase-positive– Non-lactose fermenter– Motile– Fecal-oral transmission
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSK antigen (capsular) – capsular
polysaccharideH antigen (flagellar) – single polar
flagellumEnterotoxin subunit A - stimulates cAMP
and fluid/electolyte secretionEnterotoxin subunit B – inserts subunit A
into cells
Death can occur within 12-24 hours of onset
Cholera“Rice-water” stoolsNauseaVomiting
Diagnosis– Stool Gram stain (comma-shaped rods with single
polar flagellum)– Stool culture on MacConckey agar
Treatment– Oral rehydration therapy
Vibrio parahaemolyticusCharacteristics– Gram-negative rods– Oxidase-positive– Non-lactose fermenter– Motile– Water-borne, present in undercooked
seafood
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSK antigen (capsular) – capsular
polysaccharideH antigen (flagellar) – single polar
flagellumThermostable direct hemolysin (TDH) –
cytotoxic
Mechanism not well understood, illness within 24 hours
Gastroenteritis
Diagnosis– Stool Gram stain (comma-shaped rods with single
polar flagellum)– Stool culture on MacConckey agar
Treatment– Fluids
Vibrio vulnificusCharacteristics– Gram-negative rods– Oxidase-positive– Non-lactose fermenter– Motile– Water-borne, liver disease patients at
higher risk
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSK antigen (capsular) – capsular
polysaccharideH antigen (flagellar) – single polar
flagellum
Difficult to treat with antibiotics
Wound infectionsSepsis
Diagnosis– Gram stain (comma-shaped rods with single polar
flagellum)– Culture on MacConckey agar
Treatment– Ceftiraxone and doxycycline
Pseudomonas aeruginosaCharacteristics– Gram-negative rods– Catalase-positive– Oxidase-positive– Non-fermenter– Motile– Environmental, common cause of
nosocomial infections
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSPili – promote colonizationAlginate – forms biofilms (immune
evasion and adhesion)Pyocyanin – ROS damagePyoverdin – iron uptakeExotoxins (A,S) – cytotoxicElastase – tissue destruction
Greater risk of infection in hospitalized patients, CF patients, diabetics, IV drug users, patients with breach of airway (tracheostomy, endoscopy)
Respiratory infectionsNecrotizing bronchopneumoniaChronic respiratory tract infections
Skin infectionsBurn wound infectionsEcthyma gangrenosumFolliculitis
Community acquired infectionsKeratitis (corneal ulcers)EndophthalmitisEndocarditis – IV drug users“Hot tub” folliculitisMalignant otitis externa
Osteomyelitis UTIsSepsis
Diagnosis– Gram stain– Culture on MacConkey agar (green colonies)
Treatment– Piperacillin (with tazobactam)– Cefepime– Meropenem
Burkoholderia cepacia complexCharacteristics– Gram-negative rods– Catalase-positive– Oxidase-positive– Non-fermenter– Motile– Environmental, strictly pathogenic
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSPili – promote colonizationExotoxins (A,S) – cytotoxicElastase – tissue destruction
Patients with chronic granulomatous disease or cystic fibrosis are at risk
PneumoniaUTIsSeptic arthritisPeritonitisSepsis
Diagnosis– Gram stain– Culture on MacConkey agar
Treatment– Trimethoprim and sulfamethoxazole– Ceftriaxone– Meropenem
Burkoholderia pseudomalleiCharacteristics– Gram-negative rods– Catalase-positive– Oxidase-positive– Non-fermenter– Motile– Strictly pathogenic, environmental
endemic in Southeast Asia
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSPili – promote colonizationExotoxins (A,S) – cytotoxicElastase – tissue destruction
Tuberculosis-like symptoms in immunocompromised individuals
MelioidosisCavitary pneumoniaSepsis
Cutaneous infections
Diagnosis– Gram stain– Culture on MacConkey agar
Treatment– Trimethoprim and sulfamethoxazole– Ceftriaxone
Acinetobacter baumaniiCharacteristics– Gram-negative coccobacilli– Catalase-positive– Oxidase-negative– Non-fermenter– Motile– Environmental, common cause of
nosocomial infections in immunocompromised individuals
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSPili – promote colonizationExotoxins (A,S) – cytotoxicElastase – tissue destruction
Pulmonary infections (VAP)Wound infectionsOsteomyelitis – seen in soldiersUTIsSepsis
Diagnosis– Gram stain– Culture on MacConkey agar
Treatment– Ampicillin and sulbactam– Ticarcillin and clavulanate– Trimethoprim and sulfamethoxazole
Stenotrophomonas maltophiliaCharacteristics– Gram-negative rods– Catalase-positive– Oxidase-negative– Non-fermenter– Motile– Environmental, common cause of
nosocomial infections
Virulence Factors Pathogenesis Clinical Findingsunknown Cystic fibrosis patients at
riskPneumoniaWound infectionsUTIsEndocarditisMeningitisSepsis
Diagnosis– Gram stain– Culture on MacConkey agar
Treatment– Trimethoprim and sulfamethoxazole
Neisseria gonorrhoeaeCharacteristics– Gram-negative cocci in pairs– Catalase-positive– Oxidase-positive– Non-motile– Facultatively intracellular– Strictly pathogenic
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSK antigen (capsular) – capsular
polysaccharidePili – promote colonizationOpa proteins – promote adherencePorins – promote invasion
Invasive infection
Disseminated infection in individuals with complement deficiency
WomenMucopurulent cervicitisUrethral syndrome
DysuriaPyuria
Pelvic inflammatory disease
NeonatesOphthalmia neonatorumGonococcal scalp abscessesSystemic infections
MenUrethritisEpididmytis
Rectal and oropharyngeal infections
Disseminated gonococcal infectionErythematous lesions on palms and
solesGonococcal tenosynovitis
Diagnosis– Gram stain (doughnut-shaped diplococci)– Culture on chocolate agar– PCR
Treatment– Ceftriaxone– Cefepime
Neisseria meningitidisCharacteristics– Gram-negative cocci in pairs– Catalase-positive– Oxidase-positive– Non-motile– Facultatively intracellular– Strictly pathogenic
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSK antigen (capsular) – capsular
polysaccharidePili – promote colonizationIgA1 protease – cleaves Abs
Invasive infection Meningitis
Bacteremia
Meningococcemia – meningitis with sepsis
Meningococcemia rashWaterhouse-Frederichsen syndrome
-adrenal gland hemorrhage
Diagnosis– CSF Gram stain (doughnut-shaped diplococci)– CSF culture on chocolate agar
Treatment– Ceftriaxone– Cefepime– Vaccine
Haemophilus influenzaeCharacteristics– Pleiomorphic Gram-negative rods– Catalase-positive– Oxidase-positive– Non-motile– Normal respiratory flora
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSCapsule (a-f) – capsular polysaccharidePili – promote colonizationIgA1 protease – cleaves Abs
Colonizes nasopharynx
Pneumonia worse in patients with COPD
Encapsulated stains capable of invading mucosal, hematogenous distribution
Seen in H. influenzae biogroup aegyptius
EpiglottitisSinusitisPneumonia
MeningitisSeptic arthritisSepsis
Acute conjunctivitis
Diagnosis– Gram stain (GNRs)– Culture on specialized chocolate agar
Treatment– Ceftriaxone (invasive)– Amoxicillin and clavulanate (non-invasive)– Vaccine
Haemophilus parainfluenzaeCharacteristics– Pleiomorphic Gram-negative rods– Catalase-positive– Oxidase-positive– Non-motile– Normal respiratory flora
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSCapsule (a-f) – capsular polysaccharidePili – promote colonization
EpiglottitisEndocarditis
Diagnosis– Gram stain (GNRs)– Culture on specialized chocolate agar
Treatment– Ceftriaxone – Amoxicillin and clavulanate
Haemophilus ducreyiCharacteristics– Pleiomorphic Gram-negative rods– Catalase-positive– Oxidase-positive– Non-motile– Strictly pathogenic
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSCapsule (a-f) – capsular polysaccharidePili – promote colonization
Chancroid – painful genital ulcerUnilateral regional luppurative lymphadenitis
Diagnosis– Gram stain (coccobacilli)– Culture on specialized chocolate agar
Treatment– Azithromycin– Ceftriaxone
Bordatella pertussisCharacteristics– Gram-negative coccobacilli– Catalase-positive– Oxidase-positive– Non-motile– Strictly pathogenic
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSPili – promote colonizationFilamentous hemagglutinin (FHA) –
adhesionPertussis toxin (A,B) – upregulation of
cAMP, immune dysregulationExtracytoplasmic cAMP
Adherence to respiratory epithelium and release of exotoxins
Whooping cough (pertussis)Incubation (1-3 weeks)Catarrhal stage
RhinorrheaMalaiseFeverSneezing
Paroxysmal stage Paroxysmal coughs with inspiratory
whoopsVomitingAir hunger, apnea, cyanosis
Convalescent stage – resolution
SequelaeSecondary bacteria infectionPulmonary hemorrhageEncephalopathy
Diagnosis– Gram stain (GNRs)– Culture on specialized chocolate agar
Treatment– Supportive care– Erythromycin– Vaccine
Legionella pneumophilaCharacteristics– Gram-negative coccobacilli– Catalase-positive– Oxidase-positive– Motile– Facultatively intracellular– Environmental, waterborne,
immunocompromised at greater risk, outbreaks possible
Virulence Factors Pathogenesis Clinical Findings
O antigen (somatic) – cell wall LPSPili – promote colonization
Adherence to respiratory epithelium, invasion
Legionella pneumonia – lower lobar pneumonia, cavitary in immunocompromised
Legionnaire’s disease – systemic manifestations
Non-productive coughWatery diarrhea and abdominal painNeurological symptoms
Diagnosis– Legionella urinary antigen– Culture on specialized agar
Treatment– Azithromycin– Clarithromycin– Levofloxacin
Treponema pallidumCharacteristics– Gram-negative spirochete– Few membrane proteins– Motile
Virulence Factors Pathogenesis Clinical FindingsSpirochetes penetrate skin, disseminate through blood and lymphatics, divide and grow slowly
Primary syphilisChancre (lasts 3-6 weeks)
Secondary syphilisSkin manifestations
Condylomata lataMucus patchesRash on soles and palms
Systemic involvementLatencyTertiary syphilis
Cardiovascular syphilis – endarteritis obliterans of vasa vasorum, aortic aneurysms
Gummatous syphilis – benign granulomatous gummas
Late neurosyphilisMeningovascular – strokes and
seizuresParenchymatous – tabes doralis,
dementia, Argyll Roberston pupil
Congenital syphilisEarly congenital syphilis
“Snuffles” – rhinitisCondylomatous rashHepatosplenomegalyOsteochondritis
Late congenital syphilisNeurosyphilisDeafnessKeratitisArthropathyOsteitis – saddle nose, Hutchinson’s
teeth, saber shins
Diagnosis– Darkfield microscopy– Non-treponemal tests (RPR, VDRL)– Treponemal tests
Treatment– Penicillin
LeptospiraCharacteristics– Gram-negative spirochete– Few membrane proteins– Motile
Virulence Factors Pathogenesis Clinical FindingsSpirochetes penetrate skin, disseminate through blood and lymphatics, divide and grow slowly
Primary syphilisChancre (lasts 3-6 weeks)
Secondary syphilisSkin manifestations
Condylomata lataMucus patchesRash on soles and palms
Systemic involvement
Diagnosis– Darkfield microscopy– Non-treponemal tests (RPR, VDRL)– Treponemal tests
Treatment– Penicillin
BorreliaCharacteristics– Gram-negative spirochete– Few membrane proteins– Motile
Virulence Factors Pathogenesis Clinical FindingsSpirochetes penetrate skin, disseminate through blood and lymphatics, divide and grow slowly
Primary syphilisChancre (lasts 3-6 weeks)
Secondary syphilisSkin manifestations
Condylomata lataMucus patchesRash on soles and palms
Systemic involvement
Diagnosis– Darkfield microscopy– Non-treponemal tests (RPR, VDRL)– Treponemal tests
Treatment– Penicillin
Chlamydia trachomatisCharacteristics– Gram-negative coccobacilli– Catalase-positive– Oxidase-positive– Motile– Obligate intracellular
Virulence Factors Pathogenesis Clinical Findings
No peptidoglycan Elementary bodies (Ebs) invade epithelial cells, proliferate as initial bodies (IBs), release more EBs
Serovars A-CTrachoma
Serovars D-KGenital infections
WomenCervicitisEctopic pregnancyPID
Men – epididymitisUrethritisProctitis
Infants – pneumoniaConjunctivitis
Serovars L1-L3Lymphogranulomata venereum (LGV)
Genital lesionRegional lymphadenopathyElephantiasis, fistulas, strictures
Diagnosis– Tissue cell culture– PCR (for serovars D-K, L1-L3)
Treatment– Doxycycline– Erythryomycin– Azithromycin
Chlamydia pneumoniaeCharacteristics– Gram-negative coccobacilli– Catalase-positive– Oxidase-positive– Motile– Obligate intracellular
Virulence Factors Pathogenesis Clinical Findings
No peptidoglycan Elementary bodies (Ebs) invade epithelial cells, proliferate as initial bodies (IBs), release more EBs
Atypical pneumonia
Diagnosis– Serology
Treatment– Doxycycline– Erythryomycin
Chlamydia psittaciCharacteristics– Gram-negative coccobacilli– Catalase-positive– Oxidase-positive– Motile– Obligate intracellular, common in birds
Virulence Factors Pathogenesis Clinical Findings
No peptidoglycan Elementary bodies (Ebs) invade epithelial cells, proliferate as initial bodies (IBs), release more EBs
Atypical pneumoniaFeverSplenomegaly
Diagnosis– Serology
Treatment– Doxycycline– Erythryomycin
Chlamydia psittaciCharacteristics– Gram-negative coccobacilli– Catalase-positive– Oxidase-positive– Motile– Obligate intracellular, common in birds
Virulence Factors Pathogenesis Clinical Findings
No peptidoglycan Elementary bodies (Ebs) invade epithelial cells, proliferate as initial bodies (IBs), release more EBs
Atypical pneumoniaFeverSplenomegaly
Diagnosis– Serology
Treatment– Doxycycline– Erythryomycin
Mycoplasma pneumoniaeCharacteristics– Pleiomorphic– No cell wall– Motile
Virulence Factors Pathogenesis Clinical FindingsAtypical pneumonia
Rare sequelaeStevens-Johnson syndrome –
erythema multiformeCardiac – arrhythmias, CHFNeurological – meningitis, encephalitis
Diagnosis– Cold agglutinins– Complement fixation– Sputum culture– PCR
Treatment– Doxycycline– Erythryomycin
Mycoplasma genitaliumCharacteristics– Pleiomorphic– No cell wall– Motile
Virulence Factors Pathogenesis Clinical FindingsUrethritisCervicitis
Diagnosis– Cold agglutinins– Complement fixation– Sputum culture– PCR
Treatment– Doxycycline– Erythryomycin
Mycobacterium tuberculosisCharacteristics– Pleiomorphic– No cell wall– Motile
Virulence Factors Pathogenesis Clinical FindingsUrethritisCervicitis
Diagnosis– Cold agglutinins– Complement fixation– Sputum culture– PCR
Treatment– Doxycycline– Erythryomycin
Mycobacterium lepraeCharacteristics– Pleiomorphic– No cell wall– Motile
Virulence Factors Pathogenesis Clinical FindingsTransmission unknown (believed to be respiratory droplets)
UrethritisCervicitis
Diagnosis– Cold agglutinins– Complement fixation– Sputum culture– PCR
Treatment– Doxycycline– Erythryomycin
Zoonotic Bacteria
Brucellosis Livestock Brucella Granulomatous histopathology
Leptospirosis Mammal Leptospira Fever, pulmonary hemorrhage
Cat-scratch fever Cat Bartonella Parinaud’s oculoglandular syndrome, granulomatous lymphadenitis
Plague Flea Yersinia Bubonic, pneumonic, or septicemic plague
Culture
Lyme disease Tick Borrelia Erythema migrans, early disseminated, late infection (arthritis and rarely encephalitis)
Serology
Rocky mountain spotted fever
Dog tick, wood tick
Rickettsia Lymphohistiocytic vasculitis, pulmonary and cerebral edema
Biopsy, culture, PCR
Bacterial Causes of MeningitisFirst 3
months6 months to 3 years
Adults Elderly
Listeria monocytogenesEscherichia coli
Streptococcus agalactiaeStreptococcus pneumoniaeNeisseria meningitidisHaemophilus influenzae
Within first 3 monthsListeria monocytogenesEscherichia coliStreptococcus agalactiae
6 months to 3 yearsNeisseria meningitidisHaemophilus influenzae
AdultsNeisseria meningitidisStreptooccus pneumoniae
ElderlyListeria monocytogenesNeisseria meningitidisStreptooccus pneumoniae
Bacterial Diarrheagenic Virulence Factors
Bacteria O antigen
K antigen
H antigen
Shiga toxin
Cholera toxin
Heat-labile toxin
Heat-stabile toxin
Invasive
Bacillus cereus
Listeria monocytogenesSTEC/EHEC
EIEC
ETEC
Vibrio cholerae
Salmonella
Shigella
Campylobacter
Yersinia enterocolitica
dsDNA viruses
Herpesviruses
Herpes simplex viruses (HSV-1 and
HSV-2)Varicella-zoster virus
Cytomegalovirus Epstein-Barr virus
Roseolovirus (HHV-6 and HHV-7)
Kaposi’s sarcoma-associated herpes
virus (KSHV/HHV-8)
Hepadnaviruses
Hepatitis B virus
Adenoviruses Papillomaviruses
High risk papillomaviruses
(HPV-16 and HPV 18)
Low-risk papillomaviruses
(HPV-6 and HPV-11)
Polyomaviruses
BK polyoma virus
JC polyomavirus
ssDNA viruses
Parvoviruses
Erythrovirus (parvovirus B-19)
Dependoviruses (adeno-associated
viruses)
Bocavirus
DNA Viruses
CapsulatedNon-capsulated
dsRNA viruses
Reoviruses
Rotavirus
Negative-strand ssRNA viruses
Orthomyxoviruses
Influenza viruses
Deltaviruses
Hepatitis D virus
Paramyxoviruses
Respiratory synctial virus (RSV)
Parainfluenza viruses
Human metapneumovirus Mumps virus
Measles virus
Rhabdoviruses
Rabies virus
Double-Stranded and Negative-Strand RNA Viruses
CapsulatedNon-capsulated
Positive-strand ssRNA viruses
Picornaviruses
Enteroviruses
Coxsackieviruses (A and B)
Poliovirus
Echoviruses
Rhinoviruses Hepatitis A virus
Caliciviruses
Hepatitis E virus
Norwalk virus
Togaviruses
Rubella virus
Alpha viruses (equine
encephalitis)
Flaviviruses
West Nile virus (WNV)
Yellow fever virus
Dengue fever virus
Hepatitis C virus
Coronaviruses
SARS
Positive-Strand Viruses
CapsulatedNon-capsulated
Respiratory VirusesVirus Clinical Findings
Influenza Orthomyxovirus (- ssRNA)
Headache, fever, nonproductive cough, sore throat, no rinorrhea; interstitial pneumonitis and secondary bacterial pneumonia potential complications
Parainfluenza Paramyxovirus (-ssRNA)
Croup in children
Respiratory syncytial virus
Paramyxovirus (-ssRNA)
Otitis media, bronchitis, croup, pneumonia, lower respiratory tract infections (dyspnea, hypoxemia)
Human metapneumovirus
Paramyxovirus (-ssRNA)
Similar to RSV, in children
Measles (rubeola) Paramyxovirus (-ssRNA)
Respiratory infection -> lymph nodes -> primary viremia -> endothelium -> secondary viremia (symptomatic)Fever, cough, coryza, conjunctivitis, Koplik spots, rash
Mumps Paramyxovirus (-ssRNA)
Inflammation of glandular epithelium – parotitis, orchitis; pancreatitis, ovarian infection, and meningitis infequent
Rubella (German measles)
Togavirus (+ ssRNA)
Rash, sniffles, mild lymphadenopathyCongenital rubella syndrome – spontaneous abortion, mental retardation, heart defects, cataracts and blindness
Respiratory Virus SeasonalitySpring Summer Fall Winter
Rhinoviruses
Enteroviruses
Adenoviruses
Influenza
Parainfluenza
RSV
Hepatitis VirusesVirus Classification Transmission Acute/Chronic Treatment
Hepatitis A Picornavirus (+ ssRNA)
Fecal-oral Acute Vaccination, pooled serum immunoglobulin
Hepatitis B Hepadnavirus (ds DNA)
Sexual, blood-borne, vertical
10% chronic, 90% asymptomatic
Vaccination, interferon
Hepatitis C Flavivirus (+ ssRNA) Blood-borne Chronic Interferon
Hepatitis D Deltavirus (- ssRNA) Sexual, blood-borne, vertical
Acute (superinfection with HBV)
Hepatitis E Calicivirus (+ ssRNA) Fecal-oral Acute
HerpesvirusesVirus Transmission Clinical Findings Treatment
Herpes simplex virus
Sexually, direct contact
Herpes labialis, genital herpes, gingivostomatitis, herpes whitlow, keratitis, encephalitisNeonatal herpes (SEM, CNS, or disseminated)
Acyclovir
Varicella zoster virus
Aerosolized respiratory droplets
Varicella (chicken pox) – systemic lesions, varicella pneumonia in adults, disseminated varicella (pneumonia and encephalitis) in immunodeficient
Herpes zoster (shingles) – lesions in innervated dermatome (dissemination in immunodeficient)
Acyclovir
Cyto-megalovirus
Sexually, person-to-person, transplacental
Healthy individuals – asymptomatic or mononucleosisCongenital – jaundice, hepatosplenomegaly, developmental
disorders if maternal primary infection, hearing loss if reactivation
Immunodeficient – retinitis, encephalitis, colitis
Gancyclovir
Epstein-Barr virus
Sexually Asymptomatic or mononucleosisMalignant transformations – Burkitt’s , Hodgkin’s, and post-transplant lymphomas, nasopharyngeal carcinoma
HHV-6, -7 Saliva Roseola infantum – lacy erythematous rash
HHV-8 (KSHV)
Sexually Kapsosi’s sarcoma – neovascular proliferation (purple lessions)Primary effusion lymphoma – in AIDS coinfection with EBV
Opportunistic Infections in HIVDisease CD4 Count
Herpes zoster virus 400
Tuberculosis 350
Oral candidiasis (thrush) 300
Pneumocystis jirovecii pneumonia 200
Cryptococcal meningitis 100
Mycobacterium avium complex 50
Cytomegalovirus 50
Fungi
Zygomycetes
Rhizopus
Ascomycetes
Dermatophytes
Microsporum
Microsporum canis
Microsporum gypseum
Trichophyton
Trichophyton tonsurans
Trichophyton rubrum
Epidermophyton floccsum
Aspergillus Pneumocystis jirovecii Dimorphic fungi
Histoplasma capsulatum
Coccidiodes immitis
Blastomyces dermatitidis
Paracoccidiodes brasiliensis
Penicillium marneffei
Sporothrix schenkii
Basidiomycetes
Cryptococcus neoformans
Deuteromycetes
Candida
Fungi
Opportunistic FungiSpecies Infection Patients Clinical Findings Pathology Treatment
Candida Mucocutaneous candidiasis
Diminished T cell function
Oropharyngeal (“thrush”), cutaneous, vulvovaginal erythematous lesions and white plaques
Yeast, hyphae, pseudo-hyphae, and germ tubes
Fluconazole
Candida Invasive candidiasis Diminished phagocytosis/ neutropenia
Candidemia, endocarditis, hepatosplenic and renal disease
Yeast, hyphae, pseudo-hyphae, and germ tubes
Amphotericin B
Zygomyces Zygomycosis Diminished phagocytosis/ neutropenia
Saprophytic colonization of TB lung cavities, rhinocerebral zygomycosis in ketoacidotic diabetics
Ribbon-like non-septate hyphae branching at right angles
Amphotericin B
Aspergillus Aspergillosis (allergic asperillosis, aspergilloma, invasive aspergillosis)
Diminished phagocytosis/ neutropenia
Allergic reactions, saprophytic colonization of TB lung cavities (fungal ball), necrotizing pneumonia, aflatoxin-mediated hepatotoxicity
Angular dichotomously branching septate hyphae
Voriconazole
Pneumocystis jirovecii
Pneumocystosis Diminished T cell function
Alveolar-interstitial pneumonia with fever, non-productive cough, dyspnea, hypoxia
Cyst-like structures on GMS
Trimethoprim-sulfamethoxazole
Cryptococcus neoformans
Cryptococcosis Diminished T cell function
Pulmonary infection, meningoencephalitis, systemic disease
Yeast with gelatinous capsule
Amphotericin B with/without fluorocysteine
Dimorphic FungiSpecies Geography Clinical Findings Yeast Mold Treatment
Coccidioides immitis
Desert soil of southwestern US
Pneumonia, disseminated disease can affect skin, bone, and meninges
Spore-filled spherules
Segmented arthroconidia
ItraconazoleFluconazoleAmphotericin B
Blastomyces dermatitidis
Near waters of north central and eastern US
Pneumonia, night sweats, weight loss, skin ulcers
Large budding yeast
Filamentous hyphae
ItraconazoleAmphotericin B
Histoplasma capsulatum
Caves near Ohio and Mississippi River Valleys
Pneumonia with tuberculosis-like granulomas (poorly formed in immunodeficient), RES dissemination possible
Tiny budding yeast in macrophages
Tuberculoid macroconidia
ItraconazoleAmphotericin B
Paracoccidioides brasiliensis
South America
Penicillium marneffei
Southeast Asia
Sporothrix schenkii
Global distribution
ProtozoaSpecies Transmission Clinical Findings Diagnosis Treatment
Leishmania Sandfly, rarely IV or blood transfusion
Mucosal – ulcers, can lead to bone destruction in face
Cutaneous – ulcerSystemic – spread through RES;
fever, chills, Kala-azar, hepatosplenomegaly
Biopsy of skin, blood, spleen, or liver
StibugluconateAmphotericin BMilefosine
Trichomonas vaginalis
Sexually transmitted
Men – usually asymptomatic, epidydimitis, prostatitisWomen – dysuria, foul-smelling discharge, pruritus, PID
Discharge and urine O&P
Metronidazole
Entamoeba histolytica
Ingested, rarely sexually (MSM)
Bloody diarrhea, liver abscesses Stool O&P, CT for liver abscesses
MetronidazoleTinidazole
ProtozoaSpecies Transmission Clinical Findings Diagnosis Treatment
Toxoplasma Cat feces or undercooked beef or pork
Primary infection – asymptomatic or mononucleosis in adults, seizures (CNS) and blindness (chorioretinitis) congenitallyReactivation – brain lesions, encephalitis, chorioretinitis, pneumonia, myocarditis in immunocompromised
Serology or CT
Sulfadiazine and pyrimethamine
Crypto-sporidium
Contaminated food and water, person-to-person
Watery diarrhea, vomiting, abdominal pain, for > 2-3 weeks in immunocompromised
Stool O&P with AFB
Self-limited in immunocompetent individuals
Giardia lamblia
Contaminated food and water, person-to-person
Foul-smelling greasy diarrhea, bloating, malabsorption
Stool O&P MetronidazoleTinidazoleNitazoxanide
Enterobius (Pinworm)
Transmission• Ingestion of eggs (autoinfection possible)
Clinical Presentation• Pruritus ani• Eczematous perianal lesions
Diagnosis• Scotch tape test
Treatment•Mebendazole• Pyrantel pamoate• Ivermectin
Ascaris (Roundworm)Transmission• Ingestion of embryonated eggs from soil
Clinical Presentation• Loeffler’s syndrome (eosinophilic pneumonitis)• Abdominal cramps• Gastrointestinal/biliary obstruction•Malabsorption
Diagnosis• Stool O&P
Treatment•Mebendazole• Albendazole• Ivermectin• Nitazoxanide• Pyrantel pamoate
Trichuris (Whipworm)Transmission• Ingestion of embryonated eggs from soil
Clinical Presentation• Abdominal pain• Diarrhea• Rectal prolapse• Anemia
Diagnosis• Stool O&P
Treatment•Mebendazole• Albendazole
Ancylostoma duodenale and Necator americanus (Hookworm)
Transmission• Cutaneous penetration of larvae
Clinical Presentation• Papulovesicular dermatitis (ground itch)• Loeffler-like syndrome• Diarrhea• Abdominal pain•Weight loss• Iron-deficency anemia
Diagnosis• Stool O&P
Treatment•Mebendazole• Pyrantel pamoate• Albendazole
StrongyloidesTransmission• Cutaneous penetration of larvae (autoinfection
possible)
Clinical Presentation• Loeffler-like syndrome•Larva currens (urticarial rash at site of autoinfection)•Diarrhea•Anemia•Weight loss•Hyperinfection in immunocompromised
Diagnosis•Stool O&P
Treatment•Ivermectin•Albendazole•Thiabendazole
TrichinellaTransmission• Ingestion of encysted larvae from pork
Clinical PresentationEnteral phase• Fever• Abdominal pain• Diarrhea
Diagnosis• Stool O&P
Treatment• Albendazole•Mebendazole• Thiabendazole
Parenteral phase•Myalgia•Myocarditis and arrhythmias (rare)• CNS symptoms (rare)
ToxocaraTransmission• Ingestion of embryonated eggs from soil or meat
Clinical PresentationOcular larva migransVisceral larva migrans• Hepatosplenomegaly• Bronchospasm and wheezing• CNS symptoms•Myocarditis• Nephritis
Diagnosis• Serology
Treatment• Albendazole•mebendazole• Corticosteroids
Dracunculus medinensis (Guinea worm)
Transmission• Ingestion of contaminated water
Clinical Presentation• Painful blistering ulcer• Edema• Nausea and vomiting• Fever
Diagnosis• Cutaneous emergence of worm
Treatment• Removal of worm
SchistosomaTransmission• Cutaneous penetration of larvae in water
S. haemotobium• Pruritic rash at site of
infection• Hematuria• Squamous cell carcinoma• Pulmonary hypertension• CNS symptoms
Clinical PresentationS. japonicum and S. mansoni• Pruritic rash at site of
infection• Katayama fever• Hepatosplenomegaly• Liver fibrosis• Portal hypertension• Pulmonary hypertension• CNS symptoms
Diagnosis• Stool or urine O&P
Treatment• Praziquantel
TaeniaTransmission• Ingestion of larvae in beef (T.
saginata) or pork (T. solium) or fecal-oral ingestion of eggs (cysticercosis)
Clinical PresentationT. saginata and T. solium• Diarrhea•Weight loss
Cysticercosis • Blindness• CNS symptoms
Diagnosis• Stool O&P• CT for cystericosis
Treatment• Praziquantel
CysticercosisTapeworms
Echinococcus
Transmission• Ingestion of fertilized eggs
Clinical Presentation• Calcified hydatid cysts in lungs and liver
• Abdominal pain• Biliary obstruction• Cough and chest pain• Severe allergic reaction
Diagnosis• CT• Ultrasound• Serology
Treatment• Albendazole•Mebendazole• Surgical removal of cysts
FilariasisSpecies Infection Filariae Microfilariae Vector
Wuchereria bancrofti
Lymphatic filariasis (fever, lymphadenopathy), elephantiasis
Lymphatics Blood at night Mosquito
Brugia Lymphatic filariasis, elephantiasis
Lymphatics Blood at night Mosquito
Loa loa Loaiasis (eye worm) –Calabar swelling (angioedema), subconjunctival migration
Subcutaneous, eyes
Blood at day Deer fly
Oncocerca volvulus
Onchocerciasis (river blindness) – pruritic rash, dermatitis, onchocercomata (subcutaneous nodules), blindness
Subcutaneous Skin, eyes Black fly
Vaccines
• Influenza– Inactivated virus– Live attenuated virus
• Hepatitis A– Inactivated vaccine
• Hepatitis B– Recombinant vaccine
Modes of Transmission• Sexual
– Neisseriea gonorrhoeae– Treponema pallidum– Chlamydia trachomatis– Haemophilus ducreyi– Klebsiella granulomatis– HIV– Hepatitis B– Hepatitis D– Herpes simplex virus– Cytomegalovirus– Epstein-Barr virus– Trichomonas vaginalis
• Bloodborne– HIV– Hepatitis B– Hepatitis C– Hepatitis D– Cytomegalovirus
• Foodborne– Listeria monocytogenes (dairy)– Brucella (dairy)– Bacillus anthracis– Bacillus cereus (reheated rice)– Clostridium botulinum (improper canning, fresh honey for infants)– Clostridium perfringens (undercooked pork)– Yersinia enterocolitica (undercooked pork)
– Campylobacter (undercooked chicken)– Salmonella (undercooked chicken)– Vibrio parahaemolyticus (seafood)– Escherichia coli– Taenia solium (undercooked pork)– Taenia saginata (undecooked beef)– Trichinella (undercooked meat)– Toxoplasma (undercooked meat)
• Waterborne– Vibrio cholerae– Salmonella– Legionella
• Fecal-oral– Hepatitis A– Hepatitis E– Poliovirus– Enterovirus
• Respiratory– Parvovirus B-19– Varicella zoster virus– Bacillus anthracis
• Cutaneous– Bacillus anthracis– Vibrio vulnificus
• Zoonotic
• Viral TransmissionPlacentalHIV, HBV, HDV, HCV, Rubella (before 4th mo. of preg), CMV, VZV (rarely), HSV-1,2 (rarely),Fecal/OralHAV, HEV, Enteroviruses (Poliovirus, Cocksackie, Echo)InhalationOrthomyxovirus (influenzae), Paramyxoviridae (parainfluenza, RSV, Mumps, Measles), VZV, Adenovirus, Parvovirus B19 (fifths disease), Rubella, RhinovirusMucocutaneous ContactHSV-1,2, HPV (only inoculates dividing cells), Oral SecretionsHSV-1,2, HHV, EBV, CMV (and urine)Arthropod VectorsFlaviviridae (WNV, Yellow Fever, Japanese Encephalitis and Dengue) “mosquitoes like the flavor of blood,” Alphaviridae (Chickunganya, EEE, WEE...)
Bacterial TransmissionPerson to Person– Shigella, Cryptosporidium, STEC/EHEC,
•PlacentalSyphillis (after 4th mo. of preg.) InhalationAnthrax, C. Diptheriae, Nocardia, TB, Bordatella, Legionella Furry VectorBartonella hensalae (cat bite),Arthropod VectorBorrelia burgforferi (ixodes vector), Yersinia pestis (flea vector), RMSF (dermacantor vector)Animal UrineLeptospirosis
Parasite TransmissionPlacentalToxoplasmosis Ingestion of Eggs in PorkTaenia solium, Trichinella, ToxoplasmosisIngestion of Eggs in Beef MeatTaenia Saginata, ToxoplasmosisIngetion of Eggs in Water/Dirt/HandsGiardia, Cryptosporidium, Enterobius, Ascaris, Trichuris, Toxocara, Entamoeba, Toxoplasmosis,Ingest LarvaeDraculiansisInvades via SkinHookworm, Strongyloides, SchistostomaMosquito VectorFiliarisis (or fly), MalariaOther VectorLeishmaniasis (sandfly),
Fungal Transmission
InhalationHistoplasmosis, Blastomyces, Rose ThornSporotrichosis
Infectious Causes of PneumoniaBacterial• Gram-positives (treat with beta-lactams if possible)
– Streptococcus pneumoniae– Staphylococcus aureus
• Gram-negatives (treat with cephalosporins)– Haemophilus influenzae– Klebsiella pneumoniae– Escherichia coli– Pseudomonas aeruginosa
• Atypicals (treat with macrolides or fluoroquinolones)– Legionella pneumophila– Mycoplasma pneumoniae– Chlamydia pneumoniae– Chlamydia psittaci
Viral
– Influenza virus– Respiratory syncytial virus– Parainfluenza virus– Adenovirus– Coronavirus
Fungal (mostly in immunocompromised)– Histoplasma capsulatum– Coccidioides immitis– Blastomyces – Pneumocystis jeroveci– Cryptococcus neoformans
Parasitic• Protozoan
– Toxoplasma (reactivation)• Helminthic
– Ascaris– Hookworm– Stronglyoides
Additional Infections• Hematogenous spread via RES
– Listeria monocytogenes– Salmonella typhi– Yersinia– Brucella– Legionella– Mycobacterium– Parvovirus
• Bloody diarrhea– STEC– EHEC– Salmonella– Campylobacter– Shigella
– Entamoeba histolytica• UTIs
– Escherichia coli– Klebsiella pneumoniae (in older
individuals)– Staphylococcus saprophyticus (in
younger individuals)• Meningitis
– Escherichia coli– Streptococcus agalactiae– Streptococcus pneumoniae– Neisseria meningitidis– Klebsiella pneumoniae– Haemophilus influenzae
Cell Wall Inhibitors
Penicillins Penicillin GPenicillin V
‘cidal Time-dependent
Hypersensitivity, GI problems
GPCs GPCs
Amino-penicillins
AmpicillinAmoxicillin
‘cidal Time-dependent
Hypersensitivity, GI problems, rash
GPCs and some GNs (H. influenzae)
GPCs
Aminoacyl-penicillins
Piperacillin ‘cidal Time-dependent
Hypersensitivity, GI problems
GPCs, GNRs, anaerobes (Pseudomonas, B. fragilis)
GPCs
Penicillinase-resistant penicillins
MethicllinOxacillin
‘cidal Time-dependent
Hypersensitivity, GI problems
Resistant GPCs GPCs
Cephalo-sporins
Cefotetan (2nd)Ceftiaxone (3rd)Cefepime (4th)Ceftaroline (5th)
‘cidal Time-dependent
Hypersensitivity, GI problems
1st gen – GPCs, GNRs2nd gen – longer half-life3rd gen – Pseudomonas4th gen – MRSA
GPCs
Carbapenems MeropenemErtapenem
‘cidal Time-dependent
GPCs, GNs, anaerobes, except MRSA, VRE
GPCs, GNs
Monobactam Aztreonam ‘cidal Time-dependent
GNs
Vancomycin ‘cidal Time-dependent
Skin rash, “red man” syndrome
Ribosomal Inhibitors
Amino-glycosides
GentamicinAmikacin
‘cidal Time-dependent
Nephrotoxicity, ototoxicity
severe GNs, synergy with beta lactams, TB
GPs and GNs
Tetracyclines TetracylcineDoxycycline
‘static Conc-dependent
Chelates calcium Broad spectrum and atypicals (Chlamydia, Lyme disease, H. pylori)
Chloram-phenicol
‘cidal‘static
Time-dependent
Bone marrow suppression
Select organismsGNs, anaerobes
Clindamycin ‘static Time-dependent
Pseudomembranous colitis
GPCs, anaerobes
Linezolid ‘static Time-dependent
Hypersensitivity, GI problems
Resistant GPs
Macrolides ErythromycinAzithromycin
‘static Time-dependent
Nausea and vomiting
Atypicals, Strep. pyogenes
Anti-MycobacterialsDrug name Mechanism Toxicity
Isoniazid Inhibits mycolic acid synthesis via a free radical active form
Hepatitis, peripheral neuropathy (preventable with vitamin B6), hypersensitivity, drug-induced lupus
Rifampin Inhibits bacterial RNA polymerase
Orange discoloration of secretions, hepatitis, flu-like hypersensitivity, light chain proteinuria
Pyrazinamide Structural analog of nictonamide
Hepatotoxicity (rare), hyperuricemia, photosensitivity dermatitis
Ethambutol Mechanism unknown Peripheral neuropathy, retrobulbar optic neuritis
P-aminosalicylic acid
Inhibits folate synthesis Hypersensitivity, GI toxicity, drug-induced rash
Dapsone Inhibits folate synthesis Hemolytic anemia, hypersensitivity
Rifabutin Inhibits bacterial RNA polymerase
Orange discoloration of secretions, hepatitis, flu-like hypersensitivity, light chain proteinuria
Sulfonamides and Quinolones
Sulfonamides Sulfamethoxazole E. coli, Nocardia Hypersensitivity, drug fever, Stevens-Johnson syndrome, neonatal toxicity (kernicterus)
Inhibit folate synthesis
Trimethoprim Rash, nausea, vomiting, anemia
Inhibit folate synthesis
Quinolones Ciprofloxacin (2nd)Moxifloxacin (4th)
1st gen – GN UTIs2nd gen – GNs, and some GPs3rd gen – GN and GPs4th gen – anaerobes
GI, CNS (hallucinations and depression), phototoxicify
Inhibit topoisomerase/ gyrase
Antivirals
Lamivudine Hepatitis B, HIV Reverse transcriptase inhibitor
Amantadine Rimantadine
Influenza Blocks virion release
ZanamivirOseltamivir
Influenza Neuraminidase inhibitor
AcyclovirGancyclovir
Herpes virus Thymidine kinase inhibitor
Foscarnet Herpes virus (CMV)
DNA polymerase inhibitor
Fomivirsen Herpes virus (CMV)
cDNA
Anti-RetroviralsDrug Class Mechanism Toxicities Resistance
Zidovudine (AZT)
Nucleoside-analog reverse transcriptase inhibitor
Thymidine analog
Bone marrow suppression (anemia and granulocytopenia), rarely myopathy and lactic acidosis/steatosis
Slow, with limited cross-resistance towards other NRTIs
Ritonavir Protease inhibitor Transition state peptidomimetic inhibitor
Nausea, vomiting and diarrhea common, fat redistribution, hepatic transaminits, parathesias, potent P450 inducer
Primary mutation is slow to develop and minor, stronger secondary mutations can accumulate
Nevirapine Non-nucleoside-analog reverse transcriptase inhibitor
Inhibits viral reverse transcriptase
Rash, Stevens-Johnson syndrome (severe diffuse body rash), hepatotoxicity, potent P450 inhibitor
Rapid and strong
Anti-FungalsDrug Mechanism Spectrum Toxicities
Amphotericin B Binds to ergosterol and forms ionic pores in cell membrane
Broad spectrum, but used only against severe Candida and Aspergillus because of toxicity
Primarily renal, but also fevers, chills, and hypotension
Fluconazole Inhibits ergosterol synthesis, makes cell membrane more permeable
Broad spectrum, but used against Candida albicans and Cryptococcus
P450 inhibitor, GI, rash
Itraconazole Inhibits ergosterol synthesis, makes cell membrane more permeable
Broad spectrum, but used against Aspergillus and Histoplasma
P450 inhibitor, GI, rash (although less prominent)
5-fluorocytosine Inhibits ergosterol synthesis, makes cell membrane more permeable
Used in combination with amphotericin B to treat Candida and Cryptococcus
Bone marrow depression, GI, reversible hepatotoxicity
Caspofungin Inhibits glucan synthesis Used to treat resistant fungi and severe Candida and Aspergillus
Few, including fever, nausea, and vomiting