Name

Basic Properties

Clinical Presentation

Lab Diagnosis

Virulence Factors

Treatment - Resistance

Quick Facts

Staphylococcus aureus

Basic *Gram (+) *Cocci *Clusters *Facultative anaerobe *Non-spore forming *Non-motile Location Normal flora of skin, oropharynx, GI tract, GU tract, nares

Infections Local 1. Skin/subcutaneous: impetigo (local, skin, small pus-filled vesicles), cellulitis (deep skin infection), abscesses (folliculitis, furuncles, carbuncles), wounds 2. Respiratory: pneumonia (nosocomial) 3. Bone/ joint: septic arthritis, osteomyelitis Systemic 1. Acute endocarditis 2. Bacteremia Toxins 1. Toxic Shock Syndrome (TSST-1): fever, hypotension, diffuse erythematous rash, system shock. 2. Scalded Skin Syndrome (exfoliatin): blisters, desquamation of skin; massive fluid loss, can lead to shock. 3. Gastroenteritis (enterotoxin B): food poisoning rapid diarrhea, vomiting; NO FEVER

Diagnosis 1. Grow in clusters 2. Blood culture positive 3. (+) Catalase test 4. (+) Coagulase test (to differentiate S. aureus from other Staphylococci) 5. Rapid growth on non-selective media; aerobic & anaerobic 6. Produces gold pigment

Structural 1. Polysaccharide capsule 2. Glycocalyx slime 3. Cell wall peptidoglycan and techoic acid 4. Protein A: binds Fc portion of IgG; prevents opsonization Enzymes (exoenzymes) 1. Catalase: counteracts O2 free radicals like neutrophil-derived H2O2 2. Coagulase: causes bloodclotting, builds insoluble fibrin capsule 3. Hemolysins & Leukocidin: damage RBCs and PMNs 4. Hyaluronidase: breaks down connective tissue 5. Lipase: breaks down fat 6. Staphylokinase: lyse clots

Treatment 1. Penicillinase-resistant penicillins (methicillin, oxacillin, nafcillin) 2. Cefazolin (surgical prophylaxis) [cephalosporin/ cephamycin class] 3. Clindamycin 4. Vancomycin (MRSA) Resistance Resistance to penicillin G and V due to "-lactamase. Increasing resistance to methicillin, nafcillin, and oxacillin (due to mutation in PBP-2 protein coded for by mecA gene). For methicillin-resistant staph aureus (MRSA), use vancomycin.

Transmission Spread through direct skinskin contact, especially in hospitals, or indirect (survive on dry surfaces for long times) Other *S. aureus is frequently implicated in bacterial abscesses. Patients with chronic granulomatous disease vulnerable. *Antibiotics not curative for Toxic Shock Syndrome or Scalded Skin Syndrome; kill bacteria, but do not clear toxin. *Endocarditis common among IV drug users

G R A M
(+)

C O C C I

Staph. epidermidis

Basic *Gram (+) *Cocci *Facultative anaerobe Location Colonizers of skin, oropharynx (mucous membranes) Basic *Gram (+) *Cocci *Facultative anaerobe Location Normal flora of skin, mucosa of GU tract

Infections 1. Infects patients with indwelling medical devices or immunocompromised. Not very virulent. 2. Bacteremia (through IV line) 3. Endocarditis (of artificial heart valve) 4. Orthopedic hardware infection Infections Urinary tract infection (2nd leading cause in young women, dysuria, pyuria: pus in urine)

Staph. saprophyticus

Toxins 1. TSST-1 (superantigen) produces cytokine storm 2. Enterotoxin A-E, G-I (endothelial damage) 3. Exfoliatin (ETA, ETB): epidermal necrolysis 4. Cytotoxins (!,",#,$) 5. Panton Valentine leukocidin ($): community-associated MRSA (CA MRSA), forms pores in leukocytes, tissue necrosis Diagnosis Structural 1. Grow in clusters 1. Polysaccharide capsule/ production of glycocalyx: 2. (+) Catalase test 3. (-) Coagulase test allows bacteria to stick to surface of plastics and metals 4. Novobiocin and protects them from sensitive phagocytosis. 2. Biofilm: can form biofilms Note: frequent on plastic devices. contaminant in blood cultures (beware of false +!) Diagnosis 1. Grow in clusters 2. (+) Catalase test 3. (-) Coagulase test 4. Novobiocin resistant

Treatment >50% methicillin-resistant Vancomycin Resistance Often resistant to antibiotics used to treat S. aureus such as most penicillins (methicillin, oxacillin) and cephalosporins Treatment 1. Penicillins 2. TMP-SMX

Transmission Nosocomial infection spread through infected catheters. Other When you see endocarditis with a prosthetic heart valve, think S.epidermidis if infection occurred within 60 days of valve replacement. Transmission *Common means of transmission is sexual activity (esp. in women); introduction of endogenous flora into sterile urinary tract *Commonly acquired in the community, not hospital

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Name Basic Properties Clinical Presentation Lab Diagnosis Virulence Factors Treatment - Resistance Quick Facts

Streptococcus pyogenes

Basic *Gram (+) *Cocci *Chains *Facultative anaerobe *Microaerophilic Location Common asymptomatic colonization (not normal flora) of upper respiratory tract and skin

Infections Local 1. Skin/subcutaneous: impetigo, erysipelas, cellulitis (cannot distinguish from staph aureus), necrotizing fasciitis 2. Respiratory: pharyngitis (strep throat), pneumonia (not as common as S.pneumoniae)

Diagnosis 1. Grows in strips 2. (-) Catalase test 3. Lancefield Grp A (group-specific cell wall antigens) 4. !-hemolytic (complete hemolysis on blood agar plate) 5. Bacitracin sensitivity 6. (+) PYR test, which forms red Systemic 1. Puerperal fever (post partum compound due to enzyme Lendometritis) pyrrolidomyl 2. Bacteremia arylamidase (5 and 6 Toxins differentiate from 1. Scarlet fever: systemic other forms of release of exotoxins A-C ! Strep) high fever, sandpaper rash 7. Rapid growth (begins on trunk and spreads on blood-rich outward), strawberry media; aerobic & tongue first 2 days, blistering anaerobic of palms and soles. 2. Toxic Shock Syndrome: cellulitis due to exotoxin A ! cytokine storm ! acute fever, shock. Immune-mediated 1. Glomerulonephritis: acute inflammation of glomeruli, proteinuria or hematuria, hypertension. Due to Strep antibodies complexing with glomeruli. 2. Rheumatic fever: carditis, inflammation of joints, skin. Untreated pharyngitis ! inflammatory T cell response, cross-linking in heart chronic damage to heart valves. Infections (in Neonates) 1. Neonatal meningitis 2. Neonatal sepsis 3. Neonatal pneumonia Infections in Adults 1. Septic arthritis 2. Sepsis 3. Cellulites

Structural 1. Hyaluronic acid capsule 2. Lipoteichoic acid: adhesion factor. 3. F protein: cell wall adhesion factor 4. M protein: causes rheumatic fever: alphahelix of two peptides coded by emm gene; antiphagocytic Enzymes 1. Streptolysin S and O: !hemolysis 2. Streptokinase: lyses blood clots, cause rapid spread of infection 3. Hyaluronidase: breaks down connective tissue, DNAse, anti-C5a peptidase Toxins Pyrogenic Exotoxins A-C

Treatment 1. Penicillin G 2. Clindamycin (for invasive Strep. pyogenes) 3. Erythromicin 4. Penicillinase-resistant penicillins (methicillin, oxacillin, nafcillin) for skin infections where S.aureus or S.epidermidis could be present. *Following rheumatic fever patients are placed on continuous prophylactic antibiotics to prevent repeat strep throat infections *If permanent heart valve damage has occurred, antibiotics are required when certain procedures are performed, due to high risk of endocarditis.

Transmission Usually spread by respiratory droplets or skin contact. Other *If patient presents with cellulitis, it is impossible to tell clinically whether it is due to S.aureus or S.pyogenes. *Valves damaged by rheumatic fever are susceptible to Enterococci or Viridans Streptococci infections. *In scarlet fever, bacteria is not located at erythematous rash, but found in the throat. Rash is a consequence of extotoxin. *Scarlet fever is one of the most common bacterial pediatric presentations of rash.

Strep. agalactiae

Basic *Gram (+) *Cocci *Facultative anaerobe Location Female lower GI, GU tracts.

Diagnosis 1. Grows in strips 2. (-) Catalase test 3. Lancefield Grp B 4. "-hemolytic 5. Bacitracin resistant 6. CAMP test, PCR

Treatment 1. Penicillin G 2. Ampicillin

Transmission Of chief clinical significance is that Strep. agalactiae can be vertically transmitted from mother to child during birth. Other Leading cause of neonatal meningitis.

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Name Basic Properties Clinical Presentation Lab Diagnosis Virulence factors Treatment - Resistance Quick Facts

Viridans streptococci

Basic *Gram (+) *Cocci *Facultative anaerobe Location Normal flora of oropharynx and GI tract, female genital tract Basic *Gram (+) *Diplococcus *Lancet shaped *Facultative anaerobe Location Upper respiratory or sinuses

Infections Local 1. Dental caries (S.mutans) 2. Brain or abdominal abscesses (S.intermedius) Systemic Bacterial endocarditis (infects previously damaged heart valves) Infections Local Most common cause of: 1. Lobar pneumonia (in community) 2. Otitis media (middle ear infection) 3. Sinusitis (sinus infection) Systemic 1. Meningitis (adult) 2. Bacteremia Infections Primarily in immunocompromised and hospitalized patients Local 1. UTI 2. Biliary tract infection Systemic 1. Endocarditis (infected heart valve) 2. Peritonitis (infection of the bowel lining)

Diagnosis 1. Grows in strips 2. (-) Catalase test 3. No Lancefield Group 4. "-hemolytic 5. Optichin resistant

Treatment Penicillin G

Other Commensal bacteria with generally low pathogenicity.

Strep. pneumoniae

Diagnosis 1. Grows in strips 2. (-) Catalase test 3. No Lancefield Group 4. "-hemolytic 5. Optichin susceptible (see 2nd pic on left) 6. Bile solubility test 7. Quellung reaction

Structural Polysaccharide capsule: prevents phagocytosis Enzymes 1. Pneumolysin: Damages both alveolar epithelial cells and pulmonary endothelial via upregulation of IL-6. 2. IgA proteases

Treatment 1. Penicillins 2. Cephalosporins 3. Vancomycin (for meningitis) Vaccine Pneumovax: vaccine with capsular polysaccharides (conjugated form for children). *Increasing resistance by bacteria to penicillin.

Other *Most common cause of community acquired (i.e. nonhospital based) pneumonia. *Risk of S.pneumoniae in persons with impaired IgG synthesis or splenectomy.

Enterococci (E. faecalis, E. faecium)

Basic *Gram (+) *Diplococcus *Facultative anaerobe Location Soil, food, water, normal flora of GI tract and female genital tract

Diagnosis 1. Grows in strips 2. (-) Catalase test 3. Lancefield Grp D 4. #-hemolytic 5. Grow in 6.5% NaCl solution and 40% bile 6. Hydrolyze esculin and PYR

Treatment 1. Ampicillin + aminoglycoside. 2. Vancomycin + aminoglycoside For VRE only! 3. Imipenem 4. Linezoid 5. Quinopristin-Dalfopristin Resistance Emerging resistance to vancomycin. Serious problem for health community.

Transmission *2nd most common cause of nosocomial infections. *Can colonize heart valves previously damaged by rheumatic fever *Infection is a frequent complication of hepatic surgery.

4 key bacteria with polysaccharide capsules (with asplenia as an increased risk factor): Strep. pneumonia (gram +) Klebsiella pneumoniae (gram -) N. meningitidis (gram -) H. influenza (gram -)

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Name Basic Properties Clinical Presentation Lab Diagnosis Virulence factors Treatment - Resistance Quick Facts

Corynebac. diphtheriae

Basic *Gram (+) *Rod shaped *V-shaped pairs (club-shaped bacilli in angular arrays) *Non-spore *Non-motile *Facultative anaerobe Location Oropharynx and respiratory tracts

Infection (due to toxin) Early Symptoms (2-5 days) Pseudomembrane formation in pharynx, malaise, sore throat, anorexia, fever Bull-neck: swollen jaw/upper neck Later Symptoms (6-10 days) Severe prostration, rapid pulse, striking pallor, coma and death Complications *Myocarditis *Polyneuritis (paralysis) *Parenchymatous degeneration *Fat infiltration *Liver necrosis *Respiratory insufficiency (esp infants) *Bacteremia does not occur. Infections Listeriosis Neonates: <5 days: disseminated granulomas, abscesses >5 days: meningitis (3rd in neonates) + septicimia Pregnant women: bacteremia, septicemia, fetal loss/neonatal meningitis, mild flu, asymptomatic Elderly/immunocompromised: sepsis + meningitis Others: acute febrile gastroenteritis

Diagnosis 1. Growth on Loeffler medium 2. Black colonies on K+ tellurite agar

Structural Pseudomembrane: forms in the tonsils and pharynx, which serves as a base from where it secretes its toxin. Toxins Diphtheria toxin: binary toxin with ADPribosylating activity that inhibits protein synthesis by inactivating elongation factor EF2 *A subunit: blocks protein synthesis by inactivating EF2 *B subunit: provides entry to heart, nerve Diptheriae obtains exotoxin from temperate bacteriophage. Enzymes 1. Hemolysin: like streplysin O; is heat-labile and antigenic. 2. Exotoxin lysteriolysin O: helps bacterial release and dissemination Toxins Endotoxin (Lipid A): ONLY gram (+) bacteria with an endotoxin!

Treatment 1. Erythromycin (or penicillin G) for 14 days 2. Co-administer with antitoxin (as an IND, DAT, from the CDC) 3. Immunize with vaccine (DPT = diptheria, pertussis, tetanus) Important to begin antibiotic treatment and therapy even before clinical cultures can be assayed. Patients are not contagious after 48 hours of antibiotic treatment.

Transmission Passed by person-to-person contact from respiratory droplets. Can infect any mucous membrane. Other Diptheria toxin gene is carried by a phage, so only lysogenic organisms cause systemic disease.

G R A M
(+)

Listeria monocytogenes

Basic *Gram (+) *Coccobacilli morphology *Non spore forming *Tumbling motility *Facultative anaerobe Location Grows intracellularly in gut epithelial cells.

Diagnosis 1. Blood culture using cold temperatures (bacteria can grow in temperatures as low as 4C) 2. "-hemolytic 3. (+) Catalase test

Treatment 1. Ampicillin +/- gentamicin 2. Penicillin 3. TMP-SMX Prevention *Wash and thoroughly cook food, especially meats. *Avoid raw milk

Transmission *Ingestion of contaminated raw milk or cheese from infected cows, or raw and processed meat products. *Passed through vagina during birth. Other Neonates, pregnant women, elderly, and immuno-comprised most at risk. Not infectious to healthy individuals. Healthy people may be transient carriers.

B A C I L L I

red = actin green = intracellular bacteria

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Name Basic Properties Clinical Presentation Lab Diagnosis Virulence factors Treatment - Resistance Quick Facts

Bacillus anthracis

Basic *Gram (+) *Rod-shaped *Spore forming *Non-motile *Facultative anaerobe Location Not endogenous to the body. Found in soil or livestock.

Infection (mostly due to spores) Local Cutaneous anthrax (95% of cases): formation of necrotic pustules with edema, painless black vesicles/ ulcers Gastrointestinal anthrax: lesions in intestines ! bloody diarrhea, abdominal pain, oropharyngeal infection (pseudomembrane), vomiting. Systemic Inhalational anthrax: Spores germinate in respiratory tract, migrate to lymph and enter bloodstream ! toxin is spread throughout body ! may cause bleeding and destruction of brain and chest organs, fever, dyspnea, non-productive cough. Without treatment, mortality is >80%.

Diagnosis 1. Can form long chains in culture 2. Detection of bacteria or toxins via serology or immunoassay.

Structural Protein capsule: PolyD-glutamic acid capsule escapes phagocytosis Binary Exotoxins A subunits *Lethal Factor (LF): Zn2+ protease that destroys MAPK kinase 1 ! disrupts signal transduction and causes cell death. *Edema Factor (EF): adenyl cyclase that increases cAMP ! increased ion/ water efflux and causes H2O loss, cell death. B subunits *Protective Antigen (PA): All forms have common B subunit. Recognizes the ATR (anthrax toxic receptor)! endocytosis to enter cell Toxins/capsule components are carried on extrachromosomal plasmids. Toxins Early Symptoms (lasts <24 hours) Heat-stable (Cereulide) emetic toxin: cyclic peptide ionopore ! disrupts mitochondrial function, causes vomiting. Later Symptoms (lasts ~24 hours) Hemolysin (Hbl) and Nhe: binary toxins that disrupt epithelial cells lining gut and cause diarrhea. C3-like toxin: ADP ribosylase for Rho family proteins of GPCRs.

Treatment 1. Oral penicillin G (for cutaneous and gastrointestinal) 2. Ciprofloxacin (quinolone) 3. Doxycycline (for inhalational) Treatment must begin immediately to avoid fatal complications. Short-term immunity is available.

Transmission Via bacterial endospores found in soil and livestock. Other *High human mortality (90100%) due to its life cycle. Can survive for years in dry earth or goatskin. *It is the only medically important bacteria with a protein capsule, rather than the standard polysaccharide capsule. *Could be used as a bioweapon because 1) spores are remarkably effective (stable, persistent, high potency) and 2) exotoxins are extremely lethal. *Pathology is primarily due to exotoxin effects but is dependent on its life cycle (sporulation)

See subterminal spores (clear)

Bacillus cereus

Basic *Gram (+) *Rod-shaped *Spore forming *Motile *Obligate aerobe Location Generally infects GI tract.

Infection (due to toxin) Early Symptoms (onset 1-8 hrs) Emesis: nausea and vomiting (this is prototypical food poisoning) Later Symptoms (onset 124 hrs) Abdominal pain, cramps, diarrhea (no fever or vomiting, so is not considered food poisoning) Complications (low yield) 1. Eye infections 2. Endocarditis 3. Meningitis 4. Osteomyelitis 5. Pneumonia

Diagnosis 1. Motile, aerobic spores 2. Presence of same serotype in feces/vomitus and food samples. 3. Presence of large numbers of single serotype associated with food-borne illness. 4. Enterotoxin expression by serology tests. Note: diagnosis usually not performed.

Treatment 1. Fluid rehydration 2. Vancomycin/ gentamicin or clindamycin (for serious infections) Prevention Proper handling of food (especially rice)

Transmission Via endospore from exogenous sources: soil, rice, and grains Properties of spores 1. Spores contain a complete copy of the genome. 2. Metabolically inert 3. Can survive harsh conditions. 4. Germinate in the presence of moisture and nutrients.

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Name Basic Properties Clinical Presentation Lab Diagnosis Virulence factors Treatment - Resistance Quick Facts

Clostridium botulinum

Basic *Gram (+) *Rod-shaped *Spore forming (subterminal) *Motile *Obligate anaerobe Location Not endogenous to the body.

Infection (due to toxin) Adults (within 18-24 hours) Botulism (food poisoning): dysopia (fixed dilated pupils, blurry vision), dizziness, dry mouth, abdominal pain, paralysis, and respiratory failure. Neonates Floppy Baby Syndrome: constipation, flaccid paralysis Fever does not occur in either case, because bacteria are not invasive. Wound Botulism (rare): Same as adult botulism but no GI involvement, longer incubation period, and potential fever. Infection (due to toxin) Early Symptoms Lockjaw, drooling, sweating, irritability, back spasms Later Symptoms Same as above + cardiac arrhythmias, profound sweating, dehydration. Incubation 4-5 days.

Diagnosis 1. Determine presence of toxin in food or patient serum/ feces. 2. Differentiate from aerobic sporeforming rods (Bacillus) by anaerobic culture

Toxins Botulinum toxin (BoNT) is a neurotoxin with: *A domain: protein specific endopeptidase that causes inhibition of vesicular exocytosis. *B domain: inhibits Ach release at skeletal neuromuscular junctions resulting in flaccid paralysis.

Treatment 1. Penicillin G or metronidazole 2. Immediately administer antitoxin 3. Immediate ventilator support (hyperbaric oxygen or intubation) Vaccine Multivalent vaccine is available.

Transmission *Soil *Spoiled meat or animal products Other *Botulism can occur in absence of bacteria (toxin release upon bacterial death).

Note distension

*Toxin gene present on lysogenized phage, not Prevention normal part of bacterial Heat food (for home canners) genome. because toxin is heat-labile.

Clostridium tetani

Note clubbing

Basic *Gram (+) *Rod-shaped *Spore forming (terminal clubbing) *Motile *Obligate anaerobe Location Not endogenous to the body.

Diagnosis 1. Same as C. botulinium. 2. Check for presence of tetanus toxin.

Toxins Tetanus toxin (TeNT) is a neurotoxin with: *A domain: protein specific endopeptidase that causes inhibition of vesicular exocytosis. *B domain: Inhibits release of inhibitory GABA or Gly in skeletal muscle resulting in muscular rigidity. Toxins Various exotoxins responsible for necrosis (A-B type enterotoxin, ADP-ribosylase).

Treatment 1. Penicillin G or tetracycline 2. Immediately give antitoxin globulin (only neutralizes serum toxin) Vaccine Prevention by immunization against toxin (part of DPT vaccine)

Transmission *Spore survive in soil Other *B domain responsible for different effects of botulinum and tetanus toxin. *For both botulinum and tetanus toxin, recovery requires regeneration of nerve ends since the toxin effects are irreversible. Transmission *Spread from contact of soil with deep skin wounds. *Found in contaminated meat products.

Clostridium perfringens

Basic *Gram (+) *Rod-shaped *Spore forming (subterminal/ ovoid) *Motile *Obligate anaerobe Location Found in human GI tract, as well as outside soil. Basic See C. perfringens

Infections Skin/subcutaneous Cellulitis (exotoxins lead to progressive necrosis, malodorous discharge, hemolysis, toxemia, shock and death), suppurative myositis, myonecrosis. All are associated with gas gangrene, characterized by crepitus. High mortality.

Diagnosis Culture and gram stain of aspirates, pus.

Treatment Immediate surgical removal of infected areas combined with: - Hyperbaric oxygen treatment - Penicillin G or clindamycin Mortality is high for patients with myonecrosis, suppurative myositis (and all subcutaneous infections).

Clostridium difficile

Gastrointestinal Gastroenteritis, food poisoning: fluid, electrolyte loss, diarrhea, and gastric pain (no fever). Self-limiting. Infections Pseudomembrane colitis: massive diarrhea (antibiotic-associated diarrhea with hemorrhagic necrosis). Looks like red inflamed mucosa with white exudates. Location Virulence can be turned on/ off; Commensals, normal part of GI maintenance of GI macrobiome important for suppression of pathogenic organisms. tract.

Diagnosis 1. Immunodetection of Toxin A and B in cytotoxic assay (in patients feces). 2. Colonoscopy for yellowish pseudomembrane.

Toxins 1. ToxA: enterotoxin 2. ToxB: cytotoxin, causes cardiac edema

Treatment 1. Withdraw clindamycin/ offending antibiotic (usually causative) 2. Apply metronidazole (IV or oral) or vancomycin (oral only, because IV doesnt reach colon).

Transmission Part of normal flora. Outgrowth of this species occurs during antibiotic treatment, and an upset of normal ecological balance.

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Name Basic Properties Clinical Presentation Lab Diagnosis Virulence factors Treatment - Resistance Quick Facts

ENTEROBACTER- Basic IACEAE *Gram (-) *Rod-shaped Normal flora *Variable motility *Escherichia *Facultative coli anaerobe or obligate aerobe Non-commensal *Salmonella Location *Shingella GI tract

Infections 1. Diarrhea is common symptom 2. Various other infections including urinary tract infections, pneumonia, and sepsis.

Diagnosis 1. Microscopic examination & Gram staining not sufficient. 2. Need selective media (EMB agar, MacConkey agar) & biochemical assays. All Enterobacteria ferment glucose.

Structural 1. O antigen (cell wall) most external component of LPS 2. K antigen (capsule) covers O antigen 3. H antigen (flagellar) subunits of bacterial flagella (only in motiles)

Resistance Many enterics can acquire resistance to antibiotics due to transferable plasmids (conjugation), similar to virulence factors.

Transmission Most enterics are part of the normal flora of the GI tract (with notable exceptions being Salmonella and Shingella). *Lactose fermenters: - Enterobacter - Escherichia - Klebsiella *Non-lactose fermenters: - Proteus - Salmonella - Shigella - Yersinia Transmission Consumption of unwashed vegetables or uncooked meat. Other *E. Coli is one of the most common causes of neonatal meningitis (others include S.agalactiae and Listeria) *Toxin genes + other virulence factors are usually from extrachromosomal sources (plasmids toxins, adhesions, invasive factors)

Escherichia coli

Basic *Gram (-) *Rod-shaped *Motile (has multiple flagella) *Facultative anaerobe *Ferments glucose *Ferments lactose

Note flagellated cells (peritrichous)

Infections Gastroenteritis 1. Enterotoxigenic (ETEC): Travelers diarrhea. Rice water consistency. Heat stable + heat labile toxins. 2. Enteroinvasive (ETIC): Destruction of epithelial cells lining colon. Bloody and purulent diarrhea. Secrete small dose of Shiga-like toxin. 3. Enterohemorrhagic (EHEC): Shiga-like toxin with Location bloody diarrhea (no Major commensal invasion). 4. Enteropathogenic (EPEC): GI species found in humans and all destruction of epithelial cells lining gut animals. 5. Enteroaggregative (EAEC): adherence to epithelial cells; prevent fluid absorption and transport ! small bowel damage. 6. Diffusely Adherent (DAEC): invasive; massive diarrhea Other Infections 1. UTI (pili): Adhere to urethra ! bladder (cystitis) ! kidney (pyelonephritis); 2. Bacteremia (K antigen): can lead to septic shock (from endotoxin) 3. Neonatal meningitis (K-1)

Diagnosis 1. Ferments lactose 2. Dark, purple, black, green metallic sheen on EMB agar 3. Pink-purple on MacConkeys agar 4. Serology (O, K, H antigens)

How to sort Gram bacilli: - Site of infection (GI, UR, LR, GU, skin) - Metabolism Toxins All enterics have endotoxin - Lactose fermentation Lac (+) EEK (Enterobacter, LPS. E. coli, Klebsiella) Lac (-) PYSS) *Virulence factors can be - Commensal (SSYV are not) acquired via horizontal - Virulence? (Constitutive, transfer: conjugation, acquired, or regulated) transduction Structural Treatment 1. O antigen (cell wall): Gastroenteritis most external component Supportive treatment until of LPS disseminated disease occurs (fluid/ electrolytes + small 2. K1 antigen: amount of glucose). inhibits phagocytosis (seen in neonatal UTI meningitis and Use TMP-SMX, fluoroquinolones bacteremia) 3. H antigen: (flagellar) subunits of bacterial Neonatal meningitis flagella (only in motiles) or bacteremia Use 3rd generation 4. Adhesins (seen in cephalosporins (ceftriaxone) UTI): promote attachment to epithelial cells. 5. Pili (fimbriae) 6. Siderophore Toxins 1. LT toxin: adenylate cyclase ! increase cAMP in lumen of intestine ! diarrhea 2. ST toxin: guanylate cyclase ! increase cGMP in lumen of intestine ! diarrhea 3. SLT toxin: inactivates 60S ribosome unit ! cell death

G R A M
(-)

B A C I L L I

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Name Salmonella spp Basic Properties Basic *Gram (-) *Rod-shaped *Motile (has single flagella) *Facultative anaerobe *Ferments glucose but not lactose Location Infects GI tract. Never considered commensal. VIBRONACEAE Vibrio cholerae Basic *Gram (-) *Curved rods *Motile (has single flagella) *Facultative anaerobe Location Infects GI tract. Never considered commensal. Clinical Presentation Infections S. enteritidis Gastroenteritis: inflammation, fever, diarrhea. S. typhi or S. paratyphi Typhoid fever: invade Peyers patches ! spread to liver, gall bladder, spleen ! bacteremia (rose spots on abdomen, fever, diarrhea, abdominal pain, liver/spleen enlargement). May resolve or progress to carrier state. Infections Diarrhea: often rice-water consistency; leads to dehydration, hypovolemic shock, and death if not treated. No abdominal pain. Non-invasive. Lab Diagnosis Diagnosis 1. Does not ferment lactose (EMB and MacConkey colorless) 2. Serotyping (over 2000 serotypes) 3. TSI - H2S, blackening at butt of test tube 4. Culturing: blood, stool, urine Diagnosis 1. Non-lactose fermenter 2. Oxidase positive 3. TSI medium used to differentiate Gram (-): acid slant (sucrose fermenter) and butt without gas. 4. TCBS: grows yellow colonies 5. Dark-field microscopy of stool motile organisms immobilized with antiserum. Virulence factors Structural 1. Adherence factors & invasion factors (invasins) 2. Capsule: promotes survival from phagocytotic catalase and superoxide dismutase. 3. Acid tolerance response (ATR): allows survival in acidic conditions like stomach or intracellular phagolysosomes. Structural 1. Fimbriae: cell attachment. 2. Siderophore: Fe binding protein for iron sequestering 3. H-antigen: flagella Enzymes Mucinase: digests endothelial mucous layer so bacteria can bind to cells. Toxins Cholera toxin: causes increase cAMP on Na transporter in endothelium. Results in hypersecretion of H2O and electrolytes. Treatment - Resistance Treatment S. enteritidis Usually self-limiting and does not require antibiotics. S.typhi or S. paratyphi (Typhoid fever) Always requires antibiotic treatment: Flouroquinolones Cephalosporin (ceftriaxone) Chloramphenicol Vaccine available for S. typhi. *S.typhi can hide in gallbladder; possibly result in necrotizing cholecystitis. Transmission Fecal-oral route (transmitted through contaminated food or water). Found in aqueous environments ! seafood V. cholerae, V. parahaemolyticus, V. vulnificus (latter associated with seafood and wound infections) ! all transmitted via fecal-oral route or contaminated food/drink Quick Facts Transmission *Fecal-oral route *Found in many animal reservoirs (poultry, farm animals) Other *Septicemia: in 5-10% of patients, esp. those with sickle cell anemia. *Patients with impaired gastric acid secretion are more susceptible.

Treatment Oral rehydration (water + electrolytes) can be sufficient. Otherwise: 1. Adults: Tetracycline 2. Pregnant women: furazolidone 3. Children: TMP-SMX Prevention 1. Maintain public hygiene. 2. Vaccines available (killed cell, toxoid = anti-cholera toxin). Live attenuated gives herd immunity.

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Name
PSEUDOMONADACAE

Basic Properties Basic *Gram (-) *Appear as rods *Motile (has flagella) *Obligate aerobe *Capsule *Phototrophic *Pyocyanic pigment Location *Ubiquitous in environment *Affects a variety of organ systems.

Clinical Presentation Infections Nosocomial infections 1. Pulmonary (bronchitis) 2. UTI 3. Bacteremia 4. Endocarditis (esp. from catheters and IV lines) 5. Burns and surgical sites Community-acquired 1. Pneumonia (CF patients) 2. External otitis media (ear infection) 3. Wounds (diabetic foot, diabetic osteomyelitis) 4. Folliculitis

Lab Diagnosis Diagnosis 1. Lactose nonfermenter 2. Oxidase positive, but does not reduce nitrates 3. Produces characteristic blue-green pigment (from blue pyocyanin and yellow fluorescein)

Virulence factors Structural 1. Pyocyanin: causes tissue damage and colors pus bluishgreen. 2. Adhesin: pili and neuramidase 3. Biofilm/ capsule: builds up, esp. in lung infections 4. H-antigen: flagella

Treatment - Resistance

Quick Facts

Pseudomonas aeruginosa

Treatment Transmission 1. Anti-pseudomonal penicillin The pathogen is + aminoglycoside opportunistic. Especially vulnerable are CF patients and immunocompromised. Examples a. Ticarcillin + tobramycin b. Piperacillin + gentamicin 2. Fluoroquinolones Resistance to P.aeruginosa rises quickly. Multiple combinations may need to be attempted. Prevention: Sanitation, isolation in hospital

Cells are surrounded by mucoid capsular material (biofilm component)

Cells in blood culture (paired and singles)

Haemophilus influenzae, parainfluenzae

Basic *Gram (-) *Small pleiomorphic rods *Facultative anaerobe Location *Infects upper respiratory tract *Commensal bacteria

Top: lung Bottom: CNS

Enzymes 1. Exotoxin A: similar to diphtheria toxin; ADP ribosylates host EF2 ! immune suppression, inhibits protein synthesis 4. Blood agar: 2. Exoenzyme S: ADP ribosylase transferase ! BE PSEUDO mnemonic (??) greenish metallic colonies with fruity tissue damage (grape) smell 3. Elastase: destroys elastin, collagen, fibrin, IgG, IgA, complement and lysozyme ! tissue damage, immune suppression 4. Phospholipase C: hemolysin, breaks down lipids and lecithin ! tissue invasion 5. Endotoxin: causes shock Infections Diagnosis Structural Local (non-encapsulated) 1. Requires Capsule: May contain PRP blood medium (polyribitol phosphate); 1. Otitis media for growth antiphagocytic 2. Sinusitis polysaccharide capsule. 3. Epiglottitis 2. Positive 4. Pneumonia diagnosis made Adhesions: pili and non-pilus 5. COPD exacerbation by presence of X adhesions and V factors Systemic (encapsulated) Enzymes 1. Meningitis: X=protoporphyrin IgA1 protease: counters complications include IX (heme factor) mucosal immunity mental retardation, V=NAD, NADP seizures, deafness, and (enzyme Toxins death cofactor) LPS: can induce violent inflammatory response Infections Chancroid: a painful genital ulcer, often associated with unilateral swollen lymph nodes that can rupture (pus). Diagnosis 1. Positive gram stain from ulcer exudate 2. Requires X factor only Same as H. influenzae

Treatment *3rd or 4th generation cephalosporins (ex. ceftriaxone) *Hib vaccine (type capsule conjugated to diphtheria toxoid) *Passive immunity (mom immunized during pregnancy to passively transfer antibodies in breast milk) Prevention Prevention by conjugating vaccine with diptheroid toxin (part of DPT vaccine) Treatment *3rd or 4th generation cephalosporins (ex. ceftriaxone) *Macrolide (azithromycin or erythromycin) *Ciprofloxacin (quinolone)

Transmission Transmitted via respiratory droplets; obligate human parasite Other *H.influenzae (capsule form) is frequently invasive, whereas the non-capsule colonizes locally. *H.influenzae is serious risk for patients with splenectomy.

Haemophilus ducreyi

Basic See H.influenzae Location Genitalia

Transmission Transmitted sexually

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Name Neisseria gonorrhoeae Basic Properties Basic *Gram (-) *Diplococci; kidney-bean shaped *Not motile *No endospores *Facultative anaerobe *Facultative intracellular Location *Genitals *Conjunctiva (esp. in neonates) Clinical Presentation Infections Local (Gonorrhoea) *Men: urethritis, few asymptomatic cases *Women: cervicitis, can lead to salphingitis or PID (endometritis, salpingitis, oophoritis), more likely to be asymptomatic *Both: pharyngitis, anorectal gonorrhea, peri-hepatitis (FitzHugh-Curtis syndrome) *Newborns: purulent conjunctivitis (opthalmia neonatorum). Passed to newborn via an infected birth canal. Systemic (Gonococcemia) Septic arthritis: bacteria invade submucosa and enters bloodstream. Leads to fever, purulent arthritis, pustular rash (not head and trunk). Lab Diagnosis Diagnosis 1. Oxidase positive 2. Catalase positive 3. Produce acid by metabolizing glucose (but NOT maltose). G for glucose and gonorrhea 4. Gram stain of urethral/cervical pus reveals tiny, gram negative bacteria within PMNs (i.e. intracellular divisions) 5. Must be grown on both selective media (Thayer-Martin, VCN medium) and nonselective (chocolate blood agar) 6. Blood culture generally positive only during first week of infection. Virulence factors Structural 1. Pili: adherence to epithelial cells; antigenic variation prevents immune response to reinfection. 2. Opa protein: attachment & penetration into host (opaque colonies) 3. Por B protein: prevents fusion of phagolysosome Enzymes IgA protease: cleaves IgA; allows transmission through mucus membranes Treatment - Resistance Treatment 1. Ceftriaxone (3rd generation cephalosporin) + doxycycline (to treat possible co-infection of Chlamydia) 2. Fluoroquinolones + doxycycline Resistance N.gonorrhoeae resistant to: 1. Penicillin (due to chromosomally mediated changes in penicillin-binding proteins and in cell wall permeability) 2. Tetracyclines 3. Erythromycin 4. Aminoglycosides 5. Some resistance to fluroquinolones (in Asia) Quick Facts Transmission *Sexually transmitted *Vertically transmitted to child at birth Other *Human is only reservoir for N.gonorrhoeae. *Most common cause of septic arthritis in sexually active adults. *N.gonorrhoeae die rapidly under dry conditions or in the presence of fatty acids. *2nd most common STD in US (after Chlamydia) Transmission Transmitted via respiratory droplets Other Neonates are protected by maternal antibodies

G R A M
(-)

intracellular and extracellular (around PMNs)

Toxins LOS endotoxin: stimulates Prevention 1. No vaccine inflammatory response 2. Recurrent infections possible and release of TNF-!. due to antigenic variations of pili 3. Condoms are effective

C O C C I

Neisseria meningitidis

inside PMNs

Basic *Gram (-) *Diplococci; kidney-bean shaped *Not motile *No endospores *Facultative anaerobe Location *Infection begins in nasopharynx. *Upon entering bloodstream can enter CNS.

Infections 1. Meningitis: abrupt headache, fever, meningeal signs *Thoraco-lumbar rigidity (cannot move neck forward) *Exaggerated reflexes 2. Meningococcemia (septicemia): symptoms include fever, arthritis, and characteristic petechial rash in lower extremities. Systemic Complications 1. Overwhelming disseminated intravascular coagulation (DIC = death is coming), with bilateral destruction of adrenal glands (WaterhouseFriderichsen syndrome) 2. Fevers, chills, malaise, headache

Diagnosis 1. Oxidase positive 2. Catalase positive 3. Produce acid by metabolizing glucose AND maltose. M for maltose and meningitis 4. Must be grown on both selective media (ThayerMartin VCN medium) and non- selective (chocolate blood agar) 5. Present in large numbers in CSF, blood, sputum 6. Capsular antigen tests not sensitive, infrequently used for ID

Structural 1. Capsule: Protects bacteria from phagocytosis 2. Pili: for adherence 3. Por B protein: prevents degranulation of neutrophils. Enzymes 1. Iron sequestering proteins: Can extract iron from transferring via a non-energy requiring mechanism 2. IgA protease: cleaves IgA; allows transmission through mucus membranes Toxins LOS endotoxin: diffuse vascular damage to tissues is due to toxin.

Treatment 1. Penicillin G (drug of choice) 2. Ceftriaxone (3rd generation cephalosporin) 3. Chloramphenicol Prevention *Prevention with vaccine *Chemoprophylaxis: ceftriaxone, rifampin

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Name Basic Properties Clinical Presentation Lab Diagnosis Virulence factors Treatment - Resistance Quick Facts

SPIROCHETES *Borrelia recurrentis *Borrelia burgdorferi *Leptospira interrogans *Treponema Pallidum (Syphilis, Bejel, Yaws, Pinta) Borrelia recurrentis

Basic *Gram (-) *Corkscrewshaped *Motile (6 axial filaments; periplasmic) *Microaerophilic (except leptospiraobligate aerobe) Location Varies Basic See Spirochetes group description *7-20 periplasmic flagella Location Varies

Infections Fever of varying severity common symptom in this group. Infections are multisystem inflammatory disorders.

Diagnosis 1. Weakly Gram (-) 2. Stain well with aniline dyes (Giemsa or Wright) 3. Some, but not all, spirochetes can be cultured. Have complex nutritional needs.

Toxins No exotoxins in this group

Treatment Tetracycline and doxycycline are most commonly used antibiotics to remedy bacteria in this group. *No vaccine for humans.

Transmission Commonly spread by arthropod vectors or their contaminants. Other Unique location of flagella in this group (periplasmic).

Infections Relapsing fever 1. Incubation (3-10 days); chills, fever, headache, muscle ache, shock; spirochetes are in the blood at this time. 2.Afebrile period (5-6 days); no organism in blood, fever subsides. 3. Relapse-2nd fever (3-10 days); fever with decreasing severity, headache, etc. Other symptoms 1. Splenomegaly & hepatomegaly common. 2. Characteristic macular rash from head to shoulders.

Diagnosis 1. Culture on Kellys medium (difficult) 2. Stain with aniline dyes (Giemsa or Wright stain)

Structural Antigenic shift: variable expression of out membrane Vmp lipoproteins allows Borrelia recurrentis to escape opsonization and phagocytosis

Treatment 1. Tetracycline (drug of choice) 2. Erythromycin (for pregnant women or young children) NOTE: Use antibiotics during afebrile period to prevent Jarsich- Herxheimer reaction (due to rapid release of endotoxin from killed bacteria in blood) Prevention 1. No vaccine available 2. Avoid exposure to ticks and lice 3. Rodent control

Transmission *Spread by bite of Borrelia-infected lice or ticks (vectors for this disease) *Lice: human only reservoir *Tick: rodents also reservoir Other *Mortality rate is low, but abortion rate for pregnant women can reach 90%.

S P I R O C H E T E S

*Transposition of genes 3. Antibody detection for surface protein via indirect causes antigenic shift immunoflourescence. *Genes are located on different linear plasmids 4. Dark-field (transposon position microscopy of blood determines sample (febrile activity/inactivity) period) Diagnosis Clinical criteria: ECM (flat, red skin lesion) with one late manifestation Lab criteria (need one of following): 1. Isolation of spirochete 2. Indirect immunoflorescence assay for IgM or IgG antibodies followed by Western blot analysis 3. Increase in antibody titer between acute and convalescent samples (ELISA)

Borrelia burgdorferi

Basic See Spirochetes group description *Largest of spirochetes Location Varies (multisystemic inflammatory disorder)

Infections (Lyme Disease) Phase 1 (10 days after bite) Erythema chromicum migrams (ECM-characteristic skin lesion at site of tick bite) with fever, headache, malaise, arthritis, lymphandenopathy, myalgia Phase 2 (weeks later): After dissemination: severe fatigue, headache, fever, malaise, arthralgia, ECM, cardiac dysfunction, CHF, aseptic nephritis, Bells palsy, some neurologic signs Phase 3 (month-years later) Persistent infection: meningoencephalitis, peripheral neuritis, cardiac-myocarditis, atrioventricular conduction.

erythema chromicum migrams (ECM)

*Best time to check for antibodies to B.recurrentis is during febrile period; best time to administer antibiotics is during afebrile period. Structural Treatment Transmission Phase 1: Doxycycline, *Spread by Ixodes deer Genome contains Amoxicillin, Cefuroxime tick (vectors for this linear chromosome Phase 2 or 3: Same as above, but disease) and multiple linear with increased intensity. *Deer are reservoir for tick and circular plasmids. (mouse is reservoir for tick larvae) Can survive without iron Treatment of neurological and musculoskeletal disease: (uses manganese) Penicillin G and Ceftriaxone Other *Most frequently Prevention diagnosed tick- based disease in the United 1. No vaccine. States 2. Avoid exposures to animals, apply insect repellant, avoid ticks. 3. Prompt removal of ticks if seen. Takes long time to transmit spirochetes.

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Name Basic Properties Clinical Presentation Lab Diagnosis Virulence factors Structural Corkscrewshaped with hooks. Allow for bacteria to burrow into tissue. Treatment - Resistance Quick Facts

Leptospira interrogans

Basic See Spirochetes group description *Corkscrewshaped with terminal hooks *Very small *Protoplasmic flagella *Obligate aerobe Location Varies (multisystemic disorder)

Infections (Leptospirosis) Overview 1. Either sub-clinical infection, a mild influenzalike febrile illness with myalgia. Can remit or progress to: 2. Severe systemic infections (Weills Disease) with fever, jaundice, renal and hepatic failure, vasculitis, myocarditis, meningitis, and death Incubation (7-14 days) Leptospira enters through broken skin, burrows through mucosa to enter blood stream and CNS. Acute phase (3-10 days) High fever, headache, nausea, muscle pain (thighs, lower back); progression into liver, kidneys and CNS cause jaundice and hemorrhage Afebrile period ! recurrence of fever: fever, leptospires in urine, development of septic meningitis, headache, neck pain, nephritis, hepatitis, skin lesions

Diagnosis 1. Does not stain well with Gram stain. 2. Culture blood or CSF (1st 7-10 days) or urine (after 10 days) on broth or agar medium Lab criteria (need one of following): 1. Use dark-field microscopy on blood 2. Thick smear with Giemsa stain 3. Microscoptic agglutination test (MAT): patient serum agglutinates live leptospires (or ELISA) 4. PCR: nuclei acid probes to detect bacterial DNA in serum, CSF, urine 1. Cutaneous lesions examined by dark-field microscopy, immunofluorescence, ELISA, silver stain

Treatment 1. Penicillin G + doxycycline (administered IV) 2. Tetracycline for renal infections Leptospirosis usually not fatal, unless liver or renal failure occurs. Prevention 1. Prevent exposures to matter contaminated with animal urine. 2. Reduce contamination by rodent control 3. Vaccinate livestock and pets 4. Difficult to control completely (due to widespread presence of bacteria in wild)

Transmission Transmitted by ingestion of food or water contaminated with urine of infected animals. *Reservoir: pet dogs, domestic livestock (slaughterhouse workers, etc.)

Treponema Pallidum (Subspecies: pallidum SYPHILIS)

Basic See Spirochetes group description *Replicate by transverse fission Location Varies usually genital areas

Primary very transmissive *Incubation: 0-3 months *Chancre: local inflammatory reaction with PMNs and macrophages (highly contagious); rolled-edge look *Ulcer takes 6 weeks to heal *Syphilis disseminated in lymphatics, blood, various organs long before appearance of chancre

Primary syphilis (chancre)

Brain biopsy

2. Serologic tests for syphilis (STS) A. Venereal Disease Secondary very transmissive Research Lab (VDRL) *2-12 weeks after chancre appears (~6 weeks after maximum sensitivity in it heals) and lasts for 4-8 weeks secondary syphilis *Any organ can be infected B. Rapid Plasma Reagin *Alopecia (RPR) *Fever, weight loss *Both are agglutination *Lymphadenopathy tests for Wasserman *Erythematous rash (palms and soles) bilateral antibody (Ag: cardiolipin) *Condyloma latum painless wart-like lesions *Lacks specificity (false +) packed with spirochetes = CONTAGIOUS *Mucous pouches in mouth, vagina, anus 3. Treponemal tests *Lesions in bone, liver kidneys confirmatory test *Constitutional symptoms (malaise, fever, etc.) A. FTA-ABS fluorescent treponemal antibody Latent rarely transmissive (congenital) absorption test *Lacks clinical evidence of infection (STS); CSF B. TP-PA T. pallidum exam must be negative to be considered latent particle agglutination *Can persist 1-40 years (early <4, late>4) C. Enzyme immune assay *Outcomes: recurrence of secondary, resolution, NOTE: no culturing tertiary techniques

Treatment TransmiTransmission 1. Benzathine penicillin *Sexual for primary, secondary, early *Blood transfusion latent syphilis *Congenital (50% aborted/ 2. Pencillin G for stillborn, 50% have congenital and late syphilis syphilitic stigmata: maculopapular rash, *If penicillin anemia, etc.) contraindicated, use: Tetracycline, or Doxycycline Note: Jarisch-Herxheimer reaction may occur in first few hours after antibiotic therapy of secondary syphilis (not reason to discontinue treatment) Prevention -No vaccine -Avoid sexual contact with infected individuals

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Tertiary not transmissive, rarely congenital *5-40 years after latency phase *Gummas of skin and bone necrotic granuloma *Cardiovascular syphilis (aneurysm, valve issue) *Neurosyphilis asymptomatic (subclinical; CSF test +), subacute (high lymphocyte, high protein, low glucose), meningiovascular (circle of Willis), tabes dorsalis (dorsal spinal cord: ataxia, general paresis, Argyll-Robertson pupil) T. endemicum BEJEL a. Primary and secondary lesions: oral mucosa b. Tertiary lesions: gummas of skin and bone T. pertenue YAWS a. Primary and secondary lesions: ulcerative skin lesions near initial site of infection; often looks like condyloma lata b. Tertiary lesions: gummas of skin and bone (severe facial disfigurement) T. carateum PINTA Flat red or blue lesions do not ulcerate (Por favor no PINTA mi CARA)

Treponema pallidum: *endemicum *pertenue *carateum

Basic See Treponema pallidum Geo Location T. endemicum Desert zones of Africa, Mid-east T. pertenue Moist tropical regions T. carateum Latin America

Diagnostics VDRL and FTA-ABS are positive

Treatment Penicillin Yaws: plastic surgery for facial disfigurement

Transmission T. endemicum Sharing of utensils T. pertenue Person-to-person contact; flies T. carateum Person-to-person contact

Bejel

Primary yaws

Pinta thigh skin lesion

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Name Basic Properties Clinical Presentation Lab Diagnosis Virulence factors Treatment Resistance
Treatment 1. Tetracycline 2. Macrolide (erythromycin, azithromycin) 3. Fluoroquinolones Resistance Cell wall inhibitors (penicillins, cephalosporins) do not work because no peptidoglycal cell wall

Quick Facts

Mycoplasma pneumoniae

Basic *No Gram stain *Mulberry-shaped (other Mycoplasma: fried egg look) *No cell wall *Motile *Obligate aerobe Location Upper respiratory tract (Other species cause GU infections: UTI, urethritis, pelvic inflammatory disease (PID), etc.)

Infections 1. Tracheobronchitis 2. Walking pneumonia (atypical pneumonia) fever with dry, nonproductive hacking cough (some white sputum) 3. Immunopathogenesis: causes polyclonal T-cell response (superantigenic response)

1. Culture: sputum, 2-3 weeks, essential for definitive diagnosis

DO NOT LOOK LIKE THIS!

Structural 1. P1 protein: adhesion factor that destroys cilia of epithelial 2. Cold agglutinins: IgM against M. cells of respiratory tract pneumoniae cause RBC agglutination 2. Sterols in cell membrane: at low temperatures poor require host cholesterol for sensitivity, specificity (cross rxn membrane formation with virus antigens) Metabolic Products 3. Complement fixation titer (CF): 1. Hydrogen Peroxide: H2O2 Ab titer against glycolipid antigens 2. Superoxide: O2 (peak: 4-6 weeks, last years) poor 3. Catalase inhibitor sensitivity, specificity 4. Enzyme Immuno Assay (EIA): Better specificity and sensitivity than CF: Ab to P1 most specific 5. DNA probes and PCR: not yet standardized Diagnosis 1. Culture: chick yolk sac (cannot grow on artificial media) 2. Serology: identify antibodies against rickettsial organism 3. Weil-Felix reaction (used, but not recommended) 4. Stain with Giemsa

Transmission *Respiratory droplets *Sex Humans are only reservoir.

RIKETTSIA *R. rickettsii *R. akari *R. prowazeckii *R. typhi *O. tsutsugamushi

Basic *Weakly Gram (-) *Rod-coccoid shape *Obligate intracellular bacteria (need ATP, cannot synthesize on its own) Location Varies

Infections Commonly presents with rash, fever, and headache. Prefers and damages endothelial cells.

Toxins No exotoxins in this group. ATP/ADP translocator

Treatment Doxycycline, Chloramphenicol

Transmission Transmitted by ticks or lice. Other R. akari: mites from house mice, Rickettsial Pox, WeilFelix negative R. typhi: rat flea, endemic typhus, OX-19 R. Tsutsugamushi: mite larvae (chiggers) scrub typhus (with eschar), OX-K Transmission Transmitted by ticks (with transovarian transmission) Other *R.rickettsii causes a rash that spreads from palms/soles to trunk vs. R.prowazeckii, which spreads from trunk outwards, but spares palms/soles. *One of three obligate intracellular bacterial parasites. The other two are R.prowazeckii and Chlamydia. Transmission *Transmitted by body louse (technically louse feces, not bite, since lice die from disease; no transovarian transmission) *Human reservoir maintained in Brill-Zinsser disease

I N T R A C E L L U L A R B A C T E R I A

Rickettsia rickettsii

Rickettsia prowazeckii

Basic Infections See Rickettsia group Rocky Mountain Spotted Fever description 1. Fever: 4-10 days after tick bite 2. Severe headache, muscle pain, lymphandenopathy Location Varies 3. Rash spreading from extremities to trunk and palms/soles, with inoculation eschar at tick bite 4. Replication in endothelial cells causes cell damage ! vasculitis. 5. Rare inoculation eschar 6. Encephalitis: leakage from blood vessels of brain Think East Coast (North Carolina) Basic Infections See Rickettsia group Epidemic typhus description 1. 10-14 day incubation period 2. Inflammation of endothelial lining of capillaries ! fever Location 3. Headache, delirium Varies 4. Rash on trunk that spreads outward; spares palm/soles. 5. Widespread vascular necrosis,

Diagnosis Micro-immuno-fluorescence (MIF) followed by Western blotting or PCR to distinguish species Weil-Felix test: insensitive, low specificity (cross reaction with Proteus); OX-19 (+), OX-2 (+) Culture: requires BSL-3 conditions

Mechanism of Replication 1. Attachment 2. Phagocytosis 3. Growth in cytoplasm by binary fission 4. Propulsion through cytoplasm through polymerization of host cell F actin (forms filopodia) 5. Release from host cell and attachment to adjacent cells

Treatment 1. Tetracycline 2. Doxycycline

Diagnosis Micro-immuno-fluorescence (MIF) followed by Western blotting or PCR Weil-Felix test: insensitive, low specificity (cross reaction with Proteus); OX-19 (+)

See R.rickettsia

Treatment Tetracycline (from class) Chloramphenicol and Doxycycline (from textbook)

15
gangrene, high mortality. Brill-Zinsser disease Latent microorganism remains within cells; reactivation of Rickettsia may cause transient, mild epidemic typhus. Mild symptoms, no rash. Infections Serovar A-C 1. Trachoma: scarring ! redirection of eyelashes to corneal surface ! corneal scarring and blindness Serovar D-K 1. Adult inclusion conjunctivitis: mucopurulent discharge 2. Neonatal conjunctivitis: mucopurulent discharge 3. Infant pneumonia 4. Urogenital infections (mucopurulent discharge) A. Men: nongonococcal urethritis, epididymitis, prostatitis B. Women: urethritis, cervicitis, pelvic inflammatory disease (PID) Serovar L1-L3 1. Lymphogranuloma venereum: papule or ulceration on genitals ! lymph nodes (pus) Other 1. Sterility, ectopic pregnancy, chronic pain after PID 2. Reiters syndrome: triad of conjunctivitis, urethritis, arthritis (caused by cross-reaction of Ab with joints) 3. Fitz-Hugh-Curtis syndrome perihepatitis 4. Respiratory infections 5. Atherosclerosis Infection Psittacosis: viral-like, ATYPICAL PNEUMONIA, with fever, dry, nonproductive cough Other *Endemic typhus should not be confused with typhoid fever.

Chlamydia trachomatis

Basic *Weakly gram (-) *Rod shaped *Obligate intracellular parasite *Energy parasites: steal ATP from host cell with ATP/ADP translocator Location Infects columnar mucal epithelium

Diagnosis 1. Molecular amplification tests most sensitive and specific tests available 2. Culture: chick yolk sacs; McCoy cells (specific, but insensitive) *Cell culture with specific stains (Giemsa, iodine staining of glycogen inclusions) 3. Antigen tests (DFA, ELISA): relatively insensitive

Mechanism of Replication 1. Attachment of elementary body (EB) 2. Upon ingestion, there is reorganization into a reticulate body (RB) inside phagosome. 3. Inclusion body undergoes binary fission. 4. There is increased growth and RNA/DNA synthesis (but requires host cell ATP). 5. Elementary body (EB) liberation. Lysis mediated by protease and intracellular Ca2+. Toxins All Chlamydiae have groupspecific LPS, but weak endotoxin activity. Major outer membrane protein (MOMP) is unique for each species (have serovar gene variants). Resistant to lysozyme (lack peptidoglycan and muramic acid); prevents phagosomelysosome fusion.

Treatment Lymphogranuloma venereum 1. Doxycycline 2. Erythromycin Ocular/Genital Infections 1. Doxycycline 2. Azithromycin Newborn conjunctivitis or pneumonia 1. Erythromycin

Transmission Transmitted by direct personal contact (often sex) Other *Most common bacterial STD. *Leading cause of neonatal conjunctivitis. *One of three obligate intracellular bacterial parasites. The other two are in the Rickettsia group.

Chlamidophila psittaci

See C. trachomatis

Diagnosis 1. Serological: examine blood for elevated titers of antibodies with complement fixation (CF) and immunofluorescence tests 2. Intracytoplasmic inclusion bodes do not stain with iodine Diagnosis 1. Serological: examine blood for elevated titers of antibodies with complement fixation (CF) and immunofluorescence tests 2. Intracytoplasmic inclusion bodes do not stain with iodine

Similar to C. trachomatis

Treatment 1. Doxycycline 2. Erythromycin

Transmission Bird feces inhaled Other morphology *Plasmid DNA *EB shape: Round, narrow periplasmic space * Multiple, variable sized inclusions per cell Transmission Respiratory route Other morphology *Plasmid DNA *EB shape: Pear-shaped, large periplasmic space * Multiple, uniform inclusions per cell

Chlamidophila pneumoniae

See C. trachomatis

Infection ATPYICAL PNEUMONIA in young adults (like C. psittaci and Mycoplasma)

Similar to C. trachomatis

Treatment 1. Doxycycline 2. Erythromycin

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Name Basic Properties Clinical Presentation Lab Diagnosis Virulence factors Treatment - Resistance Quick Facts

MYCOBACTERIA Basic *Acid fast *M.tuberculosis *Thin rods *M.leprae *Non-motile *M.avium *Non-spore *Obligate aerobe Location Varies

Infections Clinical presentation across the group varies.

Diagnosis A key feature is the presence of mycolic acid in cell wall. Contributes to acid-fastness (after stained by Ziehl-Neelsen or Kinyoun, red dye carolfuchsin cannot be washed away by mild acid or alcohol)

Structural 1. Lipid-rich cell wall: allows resistance to phagocytosis, germicides, and dryness. 2. Cord formation: allows for cell wall attachment between different mycobacteria. 3. High G+C DNA content: factor in slow replication of the group.

Treatment Varies

Transmission Varies

acid-fast

Mycobacterium tuberculosis

Basic See Mycobacteria group description *Weak Gram (+) *Catalase (+) Location Lungs

Infections Primary Tuberculosis 1. Aerosol droplets deposit in lung ! ingested by macrophages. 2. Mycolic acid cell wall allows intracellular replication. 3. Unaffected macrophages wall off infection ! caseous granulomas. May spread to other sites in body. Secondary Tuberculosis 1. Weakened T cell response ! reactivation of bacteria ! intense granuloma formation ! cavity formation allows bacteria to disseminate to lymph nodes, CNS, or blood (miliary TB). This stage of infection is lethal.

Mycobacteria do not have 1. Flagella 2. Capsule For species differentiation, use 3. Attachment pili 4. Exo or endo toxins molecular probe. Diagnosis Structural Lab criteria 1. Mycosides mycolic acid bound to carb. Ziehl-Neelsen or A. Cord Factor: only found Kinyoun stain in virulent strains; may be (Nocardia also responsible for TNF stains acid-fast. Be aware.) release B. Sulfatides: inhibit QuantiFERON test: phagolysosome fusion tests IFN-$ levels in C. Wax D: acts as an response to addition adjuvant of TB antigens (specific comes up 2. Iron siderophore negative in patients (Mycobactin) with BCG vaccine) Clinical criteria 1. PPD: TB skin test; delayed hypersensitivity reaction to TB antigen. Be aware of false negatives in AIDS patients. 2. Chest X-ray

Treatment Treat with RIPES (or RESPI) 1. Rifampin 2. Isoniazid 3. Pyrazinamide 4. Ethambutol 5. Streptomycin Must administer antibiotics over a long time. Drug resistance is a major problem. Prevention *Given the vast prevalence of tuberculosis in human population, active surveillance is necessary.

Transmission *Spread through respiratory droplets. *Humans are only reservoir. Other *Unusual in that is very slow at dividing. *Chronic inflammatory response is largely responsible for caseating necrosis.

M Y C O B A C T E R I A

3. Facultative intracellular growth: can survive and multiply inside macrophages. *BCG vaccine in endemic regions. Replication Can survive and multiply *Prophylactic/ therapeutic inside macrophages ! intervention. requires cell-mediated immunity.

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Name Basic Properties Clinical Presentation Lab Diagnosis Virulence factors Treatment - Resistance Quick Facts

Mycobacterium Basic leprae See Mycobacteria group description Location Damages skin (in peripheral areas), nerves, eyes, nose, and testes (cooler areas of body)

tuberculoid leprosy

Infections Tuberculoid Leprosy Increased cellular immune response but decreased humoral antibody response ! granuloma formation (IFN-$, IL-2 ! clearance of bacteria) ! localized damage to skin and nerves A. Difficult to isolate M. leprae from skin or blood B. Skin and nerves involved: 1 or 2 superficial unilateral lesions *few erythematous or hypopigmented plaques with flat centers and raised, demarcated borders; peripheral nerve damage with complete sensory loss Lepromatous Leprosy Increased antibody response, but decreased cellular immune response ! increase of bacteria in dermal macrophages and Schwann cells of PNS (more infectious and deadly!) A. Low cell-mediated immunity B. Organism found everywhere (organ, blood) C. Skin, nerves, eyes and tests involved bilaterally: multiple skin lumps and bumps, leonine facies, saddle nose, peripheral neuropathy, digit absorption, blindness and infertility in men (from testicular damage) *many erythematous macules, diffuse nerve involvement, patchy sensory loss Intermediate forms: BL, BB, BT Infections Clinically indistinguishable from severe M. tuberculosis. Seen most commonly in AIDS patients.

Diagnosis 1. Microscopy is sensitive for lepromatous form, NOT tuberculoid form 2. Skin or nerve biopsy must be done. Reveals acid fast bacilli (lepromatous) or granulomas (tuberculoid) *Culture not useful

See M. tuberculosis

Treatment Treat with DRC 1. Dapsone 2. Rifampin 3. Clofazimine

Transmission Exposure to respiratory secretions (less commonly through touch)

lepromatous leprosy

Mycobacterium Basic avium Same as M. tuberculosis

Diagnosis See M.tuberculosis

Structural See M.tuberculosis

Treatment 1. Clarinthromycin or azithromycin 2. Ethambutol 3. Rifabutin Use prophylactic treatment in AIDS patients.

Transmission *Inhalation *Ingestion of contaminated food or water. Rare pulmonary TB in healthy hosts. Seen in AIDS patients. Very virulent and resistant Mycobacteria.

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EXOTOXINS VERSUS ENDOTOXINS

Property Source Secreted from Cell Chemistry Location of Genes Toxicity Clinical effects Mode of action Vaccines Heat Stability Typical diseases Exotoxin Certain G (+) or G (-) Yes Polypeptide Plasmid or bacteriophages High (fatal dosage is 1 ug) Varies Varies Toxoids used as vaccines Destroyed rapidly at 60C (except staphylococcal enterotoxin) Tetanus, botulism, diphtheria Endotoxin Cell wall of G (-) only No Lipopolysaccharide (LPS) Bacterial chromosomes Low (fatal dosage is hundreds of ug) Fever and shock Induces mass production of TNF and IL-1 No toxoids, no vaccines Stable at 100C for 1 hour Meningococcemia, sepsis by G (-) rods.

TSI SLANT
Slant Alkaline (Pink) Butt Acid (yellow) Acidic (Yellow)

neither lactose nor sucrose fermented glucose fermented neither lactose nor sucrose fermented glucose not fermented

either lactose or sucrose fermented glucose fermented either lactose or sucrose fermented glucose not fermented

Unchanged (orange)

lifting, splitting, separation of agar from glass = GAS PRODUCTION o H2S results in blackening of agar

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COMMON DISEASES

UTI (most to lesser common causes) o E. coli o S. saprophyticus o Enterococci Endocarditis o S. aureus o S. epidermidis o Viridans streptococci (subacute) o Enterococci (subacute) o B. cereus (rare) Neonatal meningitis (most to lesser common causes) o S. agilactiae o E. coli o L. monocytogenes (>5 days onset) Toxin from phage o S. pyogenes (Erythrogenic toxin, Scarlet fever) o Corynebacterium diphtheria (tox gene) o Clostridium botulinum o V. cholera (CTX phage) o E.coli (Shiga-like toxin) Plasmid Virulence o E. coli LT = plasmid derived GI issues with fever GI issues WITHOUT fever Septic Arthritis o N. Gonorrohoeae o S. aureus o H. influenza Ab-free window o N. meningitidis 6mo to 2yrs o H. influenza 6mo to 3yrs (takes a few years of infections for child to develop own antibodies) Otitis media (middle, external) o S. pneumo o P. aeruginosa o H. influenza Vertical transmission o S. agalactiae o L. monocytogenes o N. gonorrhea o T. pallidum (congenital syphilis) Meningitis Causing bacteria o S. agalactiae (neonatal, 1st) S. pneumo (leading cause in adults) N. meningitides (second in adults) H. influenza (leading in 3mo-3yrs) B. cereus, rare Lysteria monocytogenes (neonatal, 3rd) E. coli (neonatal, 2nd) B. burgdorferi (aseptic meningitis) T. pallidum (subacute meningitis, with high lymphocyte count (other meningitis, high neutrophil)) Pneumonia o S. aureus o S. pyogenes o S. agilactiae o S. pneumo o RARE - B. cereus o P. aeruginosa o H. influenza (encapsulated) o Mycoplasma atypical (walking) o C. psittaci atypical o C. pneumoniae atypical Atypical pneumonia o mycoplasma o C. psittaci o C. pneumoniae Rash on Palms/soles o Treponema pallidum o R. rickettsii o Toxic Shock Syndrome (S. aureus, S.pyoge

o o o o o o o o

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OXYGEN SPECTRUM
Obligate Aerobes Gram (+) Bacillus cereus Nocardia (also weakly acid-fast) Facultative Anaerobes Staphylococcus *S.aureus *S.epidermis *S.saprophyticus Streptococcus *S.agalactiae *S.pneumoniae *Viridans streptococci Enterococci *E. faecalis *E. faecium Bacillus anthracis Corynebacterium diptheriae Listeria monocytogenes Actinomyces Enterobacteriaceae *Escherichia coli *Salmonella enteritis *Salmonella typhi *Shingella spp. Vibrio cholerae Haemophilus influenzae Haemophilus ducreyi Acid-fast (due to Mycobacterium mycolic acid) *Mycobacterium tuberculosis *Mycobacterium leprae *Mycobacterium avium Nocardia (also weakly acid-fast) No cell wall Mycoplasma pneumoniae Microaerophilic Streptococcus pyogenes Obligate Anaerobes Clostridium *C. botulinium *C. tetani Energy Parasites (lack metabolic machinery to use 02)

Gram (-)

Neisseria *N.gonorrhoeae *N.meningitis Pseudomonas aeruginosa Leptospira interrogans

Spirochetes *Borrelia recurrentis *Borrelia burgdorferi Treponema Campylobacter jejuni

Bacteroides

Rickettsia *Rickettsia rickettsii *Rickettsia prowarzeckii Chlamydia trachomatis

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Indigenous Gram Positive Aerobic Bacilli

Indigenous Anaerobic Species (lots found in GI tract in contrast to aerobic species)