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Page 1: micro notes

Microbiology

Page 2: micro notes

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

Page 3: micro notes

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

Page 4: micro notes

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

Page 5: micro notes

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

Page 6: micro notes

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

Page 7: micro notes

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

Page 8: micro notes

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

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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

Page 10: micro notes

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

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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)

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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)

Page 13: micro notes

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

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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

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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

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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

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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

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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

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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)

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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)

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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

Page 22: micro notes

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

Page 23: micro notes

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

Page 24: micro notes

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

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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

Page 26: micro notes

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

Page 27: micro notes

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

Page 28: micro notes

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

Page 29: micro notes

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

Page 30: micro notes

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

Page 31: micro notes

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

Page 32: micro notes

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

Page 33: micro notes

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

Page 34: micro notes

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

Page 35: micro notes

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

Page 36: micro notes

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

Page 37: micro notes

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

Page 38: micro notes

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

Page 39: micro notes

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

Page 40: micro notes

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

Page 41: micro notes

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

Page 42: micro notes

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)

Page 43: micro notes

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

Page 44: micro notes

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

Page 45: micro notes

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

Page 46: micro notes

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

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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

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Mycoplasma genitaliumCharacteristics– Pleiomorphic– No cell wall– Motile

Virulence Factors Pathogenesis Clinical FindingsUrethritisCervicitis

Diagnosis– Cold agglutinins– Complement fixation– Sputum culture– PCR

Treatment– Doxycycline– Erythryomycin

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Mycobacterium tuberculosisCharacteristics– Pleiomorphic– No cell wall– Motile

Virulence Factors Pathogenesis Clinical FindingsUrethritisCervicitis

Diagnosis– Cold agglutinins– Complement fixation– Sputum culture– PCR

Treatment– Doxycycline– Erythryomycin

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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

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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

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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

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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

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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

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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

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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

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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

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Respiratory Virus SeasonalitySpring Summer Fall Winter

Rhinoviruses

Enteroviruses

Adenoviruses

Influenza

Parainfluenza

RSV

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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

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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

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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

Page 80: micro notes

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

Page 81: micro notes

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

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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

Page 83: micro notes

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

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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

Page 85: micro notes

Enterobius (Pinworm)

Transmission• Ingestion of eggs (autoinfection possible)

Clinical Presentation• Pruritus ani• Eczematous perianal lesions

Diagnosis• Scotch tape test

Treatment•Mebendazole• Pyrantel pamoate• Ivermectin

Page 86: micro notes

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

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Trichuris (Whipworm)Transmission• Ingestion of embryonated eggs from soil

Clinical Presentation• Abdominal pain• Diarrhea• Rectal prolapse• Anemia

Diagnosis• Stool O&P

Treatment•Mebendazole• Albendazole

Page 88: micro notes

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

Page 89: micro notes

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

Page 90: micro notes

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)

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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

Page 92: micro notes

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

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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

Page 94: micro notes

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

Page 95: micro notes

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

Page 96: micro notes

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

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Vaccines

• Influenza– Inactivated virus– Live attenuated virus

• Hepatitis A– Inactivated vaccine

• Hepatitis B– Recombinant vaccine

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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