Staph Aureus

Clinical Presentation (infections)

Local

1. Skin/subcutaneous: impetigo, cellulitis, folliculitis, furuncles, carbuncles

2. Respiratory: pneumonia (hospital-based)

3. Bone-joint: septic arthritis,

osteomyelitis 

Systemic

1. Acute endocarditis

2. Bacteremia 

Staph Aureus

Clinical Presentation

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): rapid diarrhea, vomiting; no fever 

S. aureus

Diagnostic Criteria

1. Grow in clusters

2. Blood culture positive  

3. (+) Catalase test

4. (+) Coagulase test (to diff. S. aureus from other Staphylococci)

5. Rapid growth on non-selective media; aerobic & anaerobic 

6. Produces gold pigment on agar

S aureus

Virulence factors

Structural

1. Capsule

2. Protein A: binds Fc portion of IgG; prevents opsonization

Enzymes

1. Catalase: counteracts 02 free radicals, 

2. Coagulase: causes blood clotting 

3. Hemolysins & Leukocidin: damage PMNs

4. Hyaluronidase: breaks down connective tissue

5. Lipase: breaks down fat

6. Staphylokinase: lyse clots

Toxins

1. TSST-1: superantigen; produces cytokine storm

2. Enterotoxin A, B: cause leakage and destruction of endothelial cells.

3. Exfoliatin: serine protease; splits bridges in skin 

S aureus

Treatment & Resistance

Treatment

1. Penicillinase — resistant penicillins (methicillin, oxacillin, nafcillin)

2. Cefazolin (surgical prophylaxis)

3. Clindamycin

4. Vancomycin (MRSA)

Resistance

Resistance to penicillin G and V due to β-lactamase.

Increasing resistance to methicillin, nafcillin, and oxacillin (due to mutation in mecA gene)

Staph.

epidermidis

Basic Properties 

Basic

*Gram (+)

*Cocci

* Facultative

anaerobe

Location

Normal flora of

skin, oropharynx

S epidermidis

Clinical Presentation

Infections

1. Infects patients with indwelling medical devices or immunocompromised. 

2. Bacteremia (through IV line)

3. Endocarditis (of heart valve)

S epidermidis

Virulence factors

Structural

1. Polysaccharide capsule: allows bacteria to stick to surface of plastics and metals and protects them from phagocytosis.

2. Biofilm: can form biofilms on plastic devices

**highly resistant to antibiotics

S epidermidis

Lab diagnosis

Diagnosis

1. Grow in clusters

2. (+) Catalase

3. (-) Coagulase

4. Novobiocin sensitive

Note:frequent contaminant in blood cultures (can get false +)

S epidermidis

Tx & Resistance

Treatment

Vancomycin

Resistance

Often resistant to antibiotics used to treat S. aureus such as most penicillins (methicillin, cephalosporins) 

Staph saprophyticus

Basic properties

Basic

Gram (+)

Cocci (clusters)

Facultative anaerobe

non-spore forming

non-motile

Location

skin

mucus (oropharynx)

S saprophyticus

Lab diagnosis

Diagnosis

1. Grow in clusters

2. (+) Catalase

3. (-) Coagulase

4. Novobiocin resistant

S saprophyticus

Clinical presentation

1. Urinary tract infections(2^nd leading cause in young women – second to E. coli)

S saprophyticus

Tx & resistance

1. Penicillins

2. TMP-SMX (Bactrim)

Strep pyogenes

Basic 

Gram (+)

Cocci (pairs, chains)

aerotolerant / facultative anaerobe

non-motile

Location

Common asymptomatic colonization of upper respiratory tract (pharynx) and skin

S pyogenes

Virulence factors

Structural

1. Capsule (hyaluronic acid)– antiphagocytic

2. Cell wall

     --Lipotechoic acid(binds epithelial cells)

     --M-protein[causes Rheumatic Fever]: alpha-helix of two peptides coded by emm gene; antiphagocytic

     --F-protein: mediates adherence to epithelial cell

Toxins

Enzymes

1. Streptolysin S – oxygen stable; non-antigenic [beta hemolytic activity]

2. Streptolysin O – ASO test looks for Ab; oxygen labile; antigenic  [beta hemolytic activity]

3. Streptokinase – lyses blood clots 

Pyrogenic Exotoxins A-C (See Clinical Presentation) – can cause both scarlet fever and toxic shock syndrome

S pyogenes

Lab diagnosis

Diagnosis

1. Grows in chains

2. (-) Catalase

3. enriched-blood agar; aerobic & anaerobic

4. Lancefield Group A

5. β-hemolytic

6. Bacitracin sensitivity (other forms of Strep are not)

7. (+) PYR [red compound]

8. rapid Strep test (throat) – Group A carb [dimer of GlcNAc and rhamnose] antigen test

9. ASO test looks for Ab to streptolysin O (indicates recent infection)

S pyogenes

Clinical Presentation

(Infection)

LOCAL

1. Skin/soft-tissue

- Erysipelas:superficial skin infection (+subcut.)

- Cellulitis: deeper skin infection [cannot distinguish from Staph. aureus]

-Necrotizing fasciitis: infection of deep subcutaneous tissue [tissue death + high mortality rate] 

2. Respiratory

- Pharyngitis: “strep throat”

- Pneumonia:(not as common as Strep. pneumoniae) 

SYSTEMIC

1. Peurperal fever: post-partum endometritis

2. Bacteremia:infection of blood stream

S pyogenes

Clinical Presentation

(Toxins)

Toxins

1. Scarlet Fever:  bacteriophage lysogenizes organism(temperate bacteriophage)+ stimulates exotoxin A-C (superantigens) production

-FEVER, RASH (blanches) [trunk/neck]

2. Streptococcal Toxic Shock Syndrome: cellulitis due to exotoxin A -> cytokine storm -> acute fever, shock

Non-suppurative sequelae

1. Acute Rheumatic Fever:  inflammatory changes in heart, joints, blood vessels, skin (subcutaneous nodules)

- ONLY following untreated pharyngitis 

2. Glomerulonephritis

- can follow pharyngitis AND skin infections

-accute inflammation of glomeruli in kidney->hematuria (blood in urine), proteinuria, edema, HYPERTENSION [dark urine, swelling]

S pyogenes

Tx & resistance

Treatment

1. Penicillin G

2. Clindamycin (for invasive, necrotizing fasciitis) -> stops M-protein synthesis by inhibiting ribosomes

3.Erythromicin

4.Penicillinase-resistant penicillins (methicillin, oxacillin, nafcillin) --‐ for skin infections where S.aureus or S.epidermidis could be present.

Strep. agilactiae

Basic Properties

Basic

-Gram (+)

-Facultative anaerobe

-non-motile

- diplococci

Location

Normal flora of:

-lower GI

-lower GU

S agilactiae

Lab dx

- β-hemolytic

- Group B

- CAMP test

- Gram stain of CSF or urine

- Culture of CSF, urine, blood

S agilactiae

Clinical Presentation

- Neonatalmeningitis(most common)

- NeonatalPneumonia

- NeonatalSepsis

- Sepsis in PREGNANT WOMEN

- increasing incidence in elderly >65,

S agilactiae

Treatment

Strep pneumoniae

Basic properties

Basic

-Gram (+)

-“lancet” shaped diplococcic

-Facultative anaerobe

-non-motile

Location

-oropharynx (upper respiratory and sinuses)

-children common vectors

S pneumoniae

Virulence factors

Structural

1. Polysaccaride capsule (very important)

-anti-phagocytic

-cause of invasive disease

-vaccine directed at capsule

Enzymes

1. Pneumolysin

-damages alveolar epithelial cells + pulmonary endothelial cells

-cholesterol-dependent chymolysin

-up-regulates IL-6 in airways (inflammation)

S pneumoniae

Lab dx

Diagnosis

1. Grow in pairs (“lancet shaped”)

2. (-) Catalase

3. No Lancefield Group

4. α-hemolytic (leaves green area)

5. Optichin sensitive

S pneumonia

Infections

Infections

Local

1. Pneumonia– most common in community

2. Otitis media– middle ear infection; most common cause

3. Sinusitis– sinus infection; most common cause

Systemic

1. Meningitis(top cause in community—second is N. meningitidis 

2. Bacteremia

S pneumoniae

Tx & resistance

Treatment

1. Penicillins

2. Cephalosporins

3. Vancomycin (for meningitis)

Resistance

*world-wide problems: penicillin and macrolide antibiotic resistance

Vaccine

Pneumovax: vaccine with capsular polysaccharides (conjugated form for children)

Enterococci

(faecalis & faecium)

Basic 

Basic

-Gram (+)  Diplococci

-Facultative anaerobe

-non-motile

-E. faecalis - chains

Location

-Normal flora of GI tract

Enterococci

Lab dx

1. Grow in pairs

2. (-) Catalase

3. No Lancefield Group (previously Strep D)

4. γ-hemolytic 

5. Grows in presence of 6.5% NaCl and tolerates 40% bile salts

6. Hydrolyze esculin

Enterococci

Clinical Presentation

Infections

1. Urinary tract infections (nosocomial)

2. Endocarditis – gradual/subacute

3. Bacteremia/Biliary tract infections

4. Peritonitis – infection of lining of abdomen due to perforation of bowel

Enterococci

Tx & resistance

Treatment

1. Penicillins (ampicillin + aminoglycoside)

2. Vancomycin (see resistance)

Resistance

1. Resistant to Penicillin G

2. Developing resistance to vancomycin 

Corynebacteria diphtheriae

Basic Properties

Basic

-Gram (+)

-Bacillus

-“clubbing” with angular arrangements (V, W, Y)

-Non-spore forming

-non-motile

-Facultative anaerobe

Location

Respiratory, GU, Skin

Diptheria

Virulence factors

Structural

1. Pseudomembrane: forms in pharynx, serves as base from where it secretes toxins

Toxins

1. Diphtheria toxin: binary toxin with ADP-ribosylating activity that inhibits protein synthesis by inactivating elongation factor EF₂

*A subunit: blocks protein synthesis by inactivating EF₂

*B subunit: provides entry to heart, nerves

Diptheria

Lab dx

Diagnosis

1. Growth on Loeffler medium(12hrs, stain with methylene blue)

2. Black colonies on potassium tellurite agar

3. (+) Catalase

Diptheria

Clinical presentation

(due to toxin)

Early symptoms (2-6 days)

1. Pseudomembrane formation in pharynx, malaise, sore throat, anorexia, FEVER

2. Bull-neck: swollen jaw/upper neck

Later symptoms

Severe prostration, rapid pulse, striking pallor, coma and death

Complications

*Myocarditis, Polyneuritis, Parencymatous degeneration, Fat infiltration, Liver Necrosis

1. Erythromycin (or Penicillin G)

2. Co-administer antitoxin (DAT from CDC)

3. Immunize with VACCINE (DPT)

Listeria monocytogenes

Basic Properties

Basic

-Gram (+)

- Bacillus (3-5 in chains, cocci/rods)

-Non-spore forming

-MOTILE: Flagella – tumbling motility (@25°C)

-Facultative anaerobe

Location

GI tract (intracellularly in epithelial cells)

Listeria monoctyogenes

Virulence factors

Enzymes

1. Hemolysin: like Streptolysin O – heat labile, antigenic

2. Listeriolysin O: helps bacterial release and dissemination

Toxins

Endotoxin (Lipid A): ONLY gram (+) bacteria with endotoxin

Other

H-antigen (flagella)

Listeria

Lab dx

Diagnosis

1. Blood culture using low temperature 2.5°C and differential media

2. β-hemolytic

3. (+) Catalase

Listeria

Clinical presentation

1. Neonates: 

<5 days: disseminated granulomas, abscesses

>5 days: MENINGITIS (3^rd in neonates) + SEPTICEMIA 

2. Pregnant women: bacteremia, septicemia, fetal loss/neonatal meningitis, mild flu, asymptomatic

3. Elderly/immunocompromised: sepsis + meningitis

4. Others: acute febrile (FEVER) gastroenteritis

Listeria

Tx & Prevention

Treatment:

1. Ampicillin +/- aminoglycoside (gentamicin)

2. Penicillin

3. TMP-SMX

Prevention

*thoroughly cook food (meats!)

*avoid raw milk

Bacillus anthracis

Basic Properties

Basic

*Gram (+)

* Bacillus

*non-motile

*SPORE FORMING (central | subterminal)

*Facultative anaerobe (aerobe)

Location

Not endogenous

*Reservoir: sheep, goats, cattle, soil

Bacillus anthracis

Virulence factors

Structural [pXO2 plasmid]

Protein capsule: polymer of gamma-D-glutamic acid capsule prevents phagocytosis

Binary Exotoxins [pXO1 plasmid]

A subunits

*Lethal Factor (LF)– Zn²⁺ protease that destroys MAPK kinase 1 -> disrupts signal transduction -> cell death

*Edema Factor (EF): adenyl cyclase -> ↑cAMP -> increased H₂O/ion efflux -> H₂O loss + cell death

B subunits

*Protective Antigen (PA): All forms have common “B” subunit. Binds ANTRX1/2 to form heptamer (pore-like structure) -> endocytosis to enter cell

B anthracis

Lab dx

1. Detection of bacteria or toxins via serology or immunoassay

2. Gram stain

B anthracis

Clinical presentation

Local

1. Cutaneous anthrax (95% of cases): painless black vesicles/ulcers [5-20% mortality if untreated; <1% if treated]

2. Gastrointestinal anthrax: nausea, vomiting, FEVER, abdominal pain, bloody diarrhea, oropharyngeal infection (pseudomembrane) [50% mortality even with treatment]

Systemic

1. Inhalation anthrax: inhaled spores migrate to lymph system -> germinate to produce lethal toxins -> toxins cause bleeding and destruction of BRAIN,  CHEST ORGANS, etc. -> death [>80% mortality without treatment]

B anthracis

Treatment

1. Oral penicillin (cutaneous and gastrointestinal)

2. Ciprofloxacin [quinolone], Doxycycline (inhalation)

B cereus

Basic properties

*Gram (+)

* Bacillus

*MOTILE

*SPORE FORMING (central)

*OBLIGATE AEROBE

Location

Not endogenous, *Generally infects GI tract; 

Bacillus cereus

Virulence factors

Toxins

Heat-stable (a.k.a., Cereulide or emetic toxin): cyclic peptide ionopore -> disrupts mitochondrial function (causes food poisoning symptoms)

Hemolysin (Hbl) and Nhe: binary toxins; disrupt epithelial cells lining the gut 

Bacillus cereus

Lab dx

Diagnosis

1. Presence of same serotype in feces/vomitus and food samples

2. Presence of large numbers of single serotype associated with food borne illness.

3. Determination of enterotoxin expression via serology/biology tests

4. Motile, aerobic spores

*diagnosis usually not performed for this illness

Bacillus cereus

Clinical presentation

Infection (due to toxin)

FOOD POISONING

Early Symptoms (onset: 1-6 hrs; lasts <24 hrs)

Emesis: NAUSEA and VOMITING (no fever)

Later Symptoms (onset: 1-24 hrs; lasts ~24 hrs)

Diarrhea:ABDOMINAL PAIN, CRAMPS, and DIARRHEA (no fever, no vomiting)

OTHER INFECTIONS

*trauma/foreign body entry/indwelling devices (keratitis, endophthalmitis, panophthalmitis; systemic: endocarditis, meningitis, osteomyelitis, pneumonia)

B cereus

Treatment & prevention

1. fluid/electrolyte replacement (because self-limiting, no other treatment)

2. Vancomycin/gentamicin OR clindamycin (severe infections)

Prevention

Proper handling of food (especially rice)

Clostridium botulinum

Basic properties

Basic

*Gram (+)

* Bacillus

*SPORE FORMING (subterminal)

*MOTILE

*OBLIGATE ANAEROBE

Location

Not endogenous

C botulinum 

Virulence factors

Toxins

Botulinum toxin (BoNT):

*A Domain: protein specific endopeptidases that cause inhibition of vesicular exocytosis (BoNT: cleaves SNARE complex proteins: VAMP/synaptobrevin, syntaxin 1A, SNAP-25)

*B Domain: targets nerve terminals (BoNT: neuromuscular junctions)

-toxin inhibits Ach release

-toxin is HEAT-LABILE

Flagella (H-antigen positive)

C botulinum

Lab dx

Diagnosis

1. Detection of bacterium or toxin in food or patient serum/feces

2. differentiate from aerobic spore-forming bacilli by anaerobic culture

C botulinum

Clinical presentation

Infection (due to toxin)

Adults (within 18-24 hours)

Botulism (food poisoning): dysopia [fixed dilated pupils, blurry vision], dizziness, dry mouth, abdominal pain, muscle weakness, paralysis, respiratory failure [NO FEVER]

Neonates: Floppy Baby Syndrome: constipation, flaccid paralysis [NO FEVER]

Wound Botulism (rare): same as adults, except:

*NO GI Involvement

*longer incubation period

*potential FEVER!

C botulinum 

Treatment

Treatment

1. Metronidazole or Penicillin

2. Immediately administer multivalent ANTITOXIN (equine antiserum for adults; BIG-IV for children)

3. Immediate ventilator support (intubation or hyperbaric oxygen) 

Vaccine

Multivalent vaccine available 

Prevention

Heat food (for home canners) because toxin is heat-labile

Clostridium tetani

Basic properties

Basic

*Gram (+)

* Bacillus

*SPORE FORMING (terminal | “clubbed”)

*MOTILE

*OBLIGATE ANAEROBE

Location

Not endogenous

C tetani

Virulence factors

Tetanus toxin (TeNT):

*A Domain: protein specific endopeptidases that cause inhibition of vesicular exocytosis (TeNT cleaves VAMP/synaptobrevin)

*B Domain: targets nerve terminals (TeNT: GABAergic or Glycinergic synapses afferent to motoneurons)

-toxin inhibits GABA, glycine neurotransmitter release (both inhibitory)

-toxin is HEAT-LABILE

Flagella (H-antigen positive)

C tetani

Lab dx

1. Detection of bacterium or toxin in wound or patient serum

*culture bacterium from wound (absence does not negate diagnosis)

2. differentiate from aerobic spore-forming bacilli by anaerobic culture

C tetani

Clinical presentation

*incubation: days to weeks 

Early Symptoms

Lockjaw (risus sardonicus), drooling, sweating, irritability, back spasms (opisthotonos) 

Late Symptoms

Same as early symptoms + cardiac arrhythmias, BP fluctuations, profound sweating, dehydration

C tetani

Treatment

Treatment

1. Penicillin G (contraindicated because inhibits GABA) or Tetracycline

2. Immediately administer antitoxin (only neutralizes serum toxin, not intracellular toxin)

3. Supportive care: muscle relaxants + ventilation 

Vaccine

Prevention by immunization against toxin (part of DPT)

Clostridium perfringens

Basic properties

Basic

*Gram (+) - variable

* Bacillus

*SPORE FORMING (subterminal | ovoid)

*non-motile

*OBLIGATE ANAEROBE

Location

Endogenously found in GI tract, as well as outside soil

C perfringens 

virulence factors

Toxins

Various exotoxins (A-B type ENTEROTOXIN; ADP-ribosylase) responsible for NECROSIS

*Θ toxin – β-hemolytic

*α-toxin – α-hemolytic, lecithinase

Enzymes

Exoenzymes that cause tissue destruction

C perfringens

lab diagnosis

1. Culture and Gram stain of aspirates, pus

2. Blood culture

C perfringens

Clinical presentation

Soft Tissue

1. Cellulitis: exotoxins lead to progressive necrosis, malodorous discharge, hemolysis, toxemia, shock and death

2. Suppurativemyositis

3. Myonecrosis

*all associated with GAS GANGRENE (characterized by crepitus)

Enteric infection

1. Gastroenteritis (self-limiting): Watery diarrhea: associated with food-borne ingestion

*associated with institutional food preparation

C perfringens 

Treatment

1. debridement: immediate surgical removal of infected areas combined with

a.    hyperbaric oxygen

b.   Penicillin G or Clindamycin

*mortality high for patients with myonecrosis, suppurative myositis (and all subcutaneous infections)

Clostridium difficile

Basic properties

Basic

*Gram (+)

* Bacillus

*SPORE FORMING (subterminal | ovoid)

*MOTILE

*OBLIGATE ANAEROBE

Location

Normal flora of GI tract

C difficile

Virulence factors

Toxins

1. ToxA: enterotoxin

2. ToxB: cytotoxin – causes cardiac edema

C difficile

Lab dx

1. Detect Toxin A and B in cytotoxic assay (immunodetection in patient’s feces)

2. Colonoscopy to determine yellowish pseudo-membrane

3. isolation of bacterium in patient’s feces

C difficile

Clinical presentation

Infections

Pseudomembranous Colitis: antibiotic-associated diarrhea (with hemorrhagic necrosis) 

*looks like red inflamed mucosa with white exudates

C difficile

Treatment

Treatment

1. Withdraw offending antibiotic (commonly ampicillin or clindamycin or even cephalosporins – both broad spectrum)

2. metronidazole (IV or oral) or vancomycin (oral, because IV doesn’t reach colon)

Escherichia coli

basic properties

Basic

*Gram (-)

* Bacillus

*MOTILE (peritrichous)

*Facultative anaerobe

*ferments glucose

*ferments lactose

Location

Commensal GI species

E coli

Virulence factors

Structural

1. O antigen– external-most part of LPS

2. K-1 antigen– capsule, inhibits phagocytosis (seen in neonatal meningitis and bacteremia)

3. H antigen– flagellar, bacterial flagella subunits

4. Pili (fimbriae)

5. Adhesins

6. Siderophore

Toxins

1. LT (heat labile) toxin: adenylate cyclase -> ↑cAMP -> diarrhea

2. ST (heat stabile) toxin: guanylate cyclase -> ↑cGMP -> diarrhea

3. Shiga-like toxin: inactivates 60S ribosome unit -> cell death

E coli

Lab dx

Diagnosis

LACTOSE FERMENTERS:

1. EMB agar (dark purple, black with metallic green sheen)

2. MacConkey agar – pink-purple appearance

3. Culture (blood, urine, CSF, sputum) – can grow at 45.5°C

4. Serology – O, K, H antigens

E coli

Clinical presentation

Infection

Gastroenteritis

1. ETEC – Traveler’s diarrhea. Rice-water consistency. ST, LT toxins.

2. EIEC – invade epithelial cells, produce little Shiga-like toxin, bloodydiarrhea with WBCs (pus), FEVER

3. EPEC – adherence; small bowel damage

4. EAEC – clumping; fluid transport interference 

5. EHEC – Shiga-like toxin (inhibits 60S). Abdominal pain with bloody diarrhea(no invasion); O157:H7 – hemolytic uremic syndrome 

6. DAEC – invasive, watery diarrhea

1. UTI (pili): adhere to urethra -> bladder (cystitis) -> kidney (pyelonephritis)

2. Bactermia/sepsis (K-antigen): due to lipid A of LPS

3. Neonatal meningitis(K-1): second most common cause

E coli

Treatment

Treatment

1. Gastroenteritis: supportive treatment ONLY (fluid/electrolytes + small amt. of glucose)

2. UTI – TMP-SMX, fluoroquinolones

3. Neonatal Meningitis and Bacteremia: 3^rd generation cephalosporins (ceftriaxone)

Salmonella

Basic properties

Basic

*Gram (-)

* Bacillus

*MOTILE (peritrichous  flagella)

*Facultative anaerobe

*ferments glucose

*DOES NOT ferment lactose

Location

*Infects GI tract – NEVER CONSIDERED COMMENSAL

Salmonella

virulence factors

Structural

1. Adherence factors& invasion factors (invasins)

2. Capsule (Vi): promotes survival from phagocytic catalase and superoxide dismutase

3. Acid tolerance response(ATR) – allows survival in acidic conditions (stomach, phagolysosomes) 

4. H-antigen(flagella)

5.  Siderophores

Salmonella

lab dx

Diagnosis

1. TSI – H₂S, blackening at butt of test tube

2. No lactose fermentation (EMB and MacConkey  colorless)

3. Serotyping (over 2000 serotypes)

4. Culturing: blood, stool, urine

Salmonella

Clinical presentation

S. enteritidis

Gastroenteritis: inflammatory diarrhea (tissue invasion – lamina propria)

S. typhi/S. paratyphi

Typhoid fever: invade Peyer’s patches -> spread to liver, gall bladder, spleen -> bacteremia [rose spots on abdomen, FEVER, diarrhea, abdominal pain, liver/spleen enlargement]

*can get carrier state

Salmonella

treatment

S. enteritidis

Usually self-limiting without treatment 

S. typhi/paratyphi  fluoroquinolones, chloramphenicol, cephalosporin (e.g., ceftriaxone)

Vaccine: available for S. typhi

Vibrio cholerae

basic properties

Basic

*Gram (-) *CURVED bacillus

*MOTILE (single polar flagellum)

*Facultative anaerobe

*OXIDASE POSITIVE

*ferments sucrose

*DOES NOT ferment lactose

Location

*Infects GI tract – NEVER CONSIDERED COMMENSAL

Vibrio cholera

virulence factors

Structural

1. Fimbriae – cell attachment  2. Siderophores  3. H-antigen– flagella

Enzyme

1. Mucinase – adhesion factor, digests mucous to allow attachment

Toxin

1. Cholera toxin

*From CTX phage -> transducible through pili

A-subunit: central, ADPRase -> constitutively active adenylate cyclase -? ↑cAMP à ↑H₂O and electrolyte secretion

B-subunit: pentameric 

V cholera

Lab dx

1. Oxidase (+) 

2. No lactose fermentation (EMB and MacConkey  colorless) 

3. TSI – acid slant (sucrose fermenter) and butt without gas

4. TCBS – grows yellow colonies

5. Dark-field microscopy of stool – motile organisms immobilized with antiserum

*culture, serological, biochemical testing

V cholera

clinical presentation

Infection

Diarrhea: “rice-water” consistency, leads to hypovolemic shock (and death if not treated)

No abdominal pain

NON-INVASIVE

V cholera

Tx & prevention

Oral rehydration (water + electrolytes + glucose) can be sufficient 

Otherwise…

1. Pregnant women: furazolidone

2. Children – TMP-SMX

3. Others – tetracycline 

Prevention

*public hygiene

*Vaccines (killed cell, toxoid [anti-cholera toxin], live attenuated)

**Live attenuated gives “herd immunity”

Pseudomonas aeruginosa

basic properties

Basic

*Gram (-) Bacillus

*MOTILE

*OBLIGATE AEROBE

*OXIDASE POSITIVE

*DOES NOT ferment lactose (or any other sugar)

*Phototrophic

*CAPSULE

Location

Ubiquitous in environment; many organs affected

P aeruginosa

virulence factors

Structural

-Pyocyanin – damages tissue via ROS, blue pus

-Adhesin factors, H-antigen(flagella)

-Biofilm/capsule– problematic in lung infections

Enzymes

-Exoenzyme S– ADP ribosylase ->tissue damage

-Phospholipase C– hemolysin , breaks lipids and lecithin (tissue invasion)

-Elastase – destroys elastin, collagen, fibrin, IgG, IgA, complement, etc. 

Toxins

-Exotoxin A– increased tissue damage, invasion, immune suppression (inhibits EF₂)

P aeruginosa

lab dx

1. Oxidase (+) 

2. No lactose fermentation (EMB and MacConkey  colorless) 

3. Blue-green pigment (from blue pyocyanin and yellow fluorescein) 

4. Blood agar – greenish-metallic colonies with FRUITY (grape) smell

P aeruginosa

clinical presentation

Nosocomial

1. Burns and SurgicalSites

2. Endocarditis (catheters, IV lines), Bacteremia, Sepsis

3. Pulmonaryinfections (bronchitis – bronchopneumonia)

4. UTI 

Community

1. Pneumonia (CF patients)

2.  Externalotitismedia

3. Woundinfections (including diabetic foot, diabetic osteomyelitis)

4. Folliculitis

“BE PSEUDO” mnemonic  

 P aeruginosa

tx & prevention

Treatment

1. anti-pseudomonal penicillin + aminoglycoside

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

Haemophilus

(influenza, parainfluenza, ducreyi)

Basic properties

Basic

*Gram (-)

*Bacillus (small, pleomorphic)

*non-motile

*Facultative anaerobe

*CAPSULE

Location

H. influenza – infects upper respiratory tract

H.  ducreyi – infects genitalia 

Haemophilus

Virulence factors

Structural

1. Capsule: antiphagocytic polysaccharide capsule; may contain PRP (polyribitol phosphate)

*6 types: b most virulent

2. Adhesions: pili and non-pilus adhesions (oropharynx colonization)

Enzymes

IgA protease– counter mucosal immunity

Toxins

LPS: can induce violent inflammatory response; impair ciliary functions

Haemophilus

Lab dx

H. influenza

1. Requires X factor (poroporphyrin IX) and V factor (NAD, NADP)

2. Fastidious growth on Chocolate Agar with X, V factors

3. Satellite Phenomenon: H. influenza grows around S. aureus (which produces V factor)

4. Fluorescently labeled antibodies 

5. Positive Quellung test: due to capsule 

H. ducreyi

1. Gram (-) stain from ulcer exudate and pus

2. Only requires X factor

haemophilus

Clinical presentation

 Influenza 

Encapsulated

Meningitis – type b primary cause in infants 3mo to 3yrs old (mental retardation, seizures, deafness)

 Epiglottitis,  Pneumonia, Septicarthritis, Sepsis 

Non-Encapsulated

 Otitismedia, Sinusitis

 COPD exacerbation

H. ducreyi

Chancroid: painful genital ulcer, associated with unilateral swollen lymph nodes that can rupture (pus)

H influenza

Treatment

H. Influenza

1. 3^rd generation cephalosporins 

2. Hib vaccine (type capsule conjugated to diphtheria toxoid) 

3. Passive immunity – mother immunized during pregnancy to passively transfer antibodies in breast milk

H. ducreyi

Treatment

1. 3^rd generation cephalosporins (e.g., ceftriaxone – IM)

2. Macrolide (azithromycin or erythromycin)

3. Ciprofloxacin (quinolone)

Neisseria Gonorrhea

Basic properties

Basic

*Gram (-)

*Diplococcus (kidney/coffee bean shaped)

*Non-motile

*Facultative anaerobe

Location

*Genitalia

*Conjunctiva (esp. neonates) 

N gonorrhea

Virulence factors

Structural

1. Pili: adherence to epithelial cells; antigenic variation prevents immune response to reinfection

2. Opa protein: attachment and penetration into host [opaque colonies]

3. PorB: prevents fusion of phagyolysosome

Enzymes

1. IgA₁ Protease: cleaves IgA; allows transmission through mucous membrane

2. Iron sequestering proteins:  

Toxin

LOS endotoxin: stimulates inflammatory response and TNF-α release

N gonorrhea

Lab dx

Microscopy

Gram stain used to diagnose men with purulent urethritis and women with cervicitis – PMNs + gram (-) cocci 

Culture

1. Oxidase (+)

2. Catalase (+)

3. Must grow on selective media (TM VCN – vancomycin, colistin, nystatin) and non-selective media (Chocolate Agar)

4. ONLY FERMENTS GLUCOSE– produces acid

*die in presence of fatty acids, trace metals, dry conditions

*blood culture results only positive during first week of infection 

N gonorrhea

Clinical presentation

(often asymptomatic)

Men:  Purulent discharge, Dysuria

rare: epididymitis, prostatitis, peri-urethral abscesses, orchitis (testes)

Women: Vaginaldischarge, Dysuria, Abdominalpain

PID: endometritis (uterus), salpingitis (fallopian tubes), oophoritis (ovaries)

*complications: sterility, ectopic pregnancy,abscess, peritonitis

*Both men and women:

Pharyngitis, Anorectal gonorrhea, peri-hepatitis (Fitz-Hugh-Curtis syndrome) – can also occur in Chlamydia 

4. Newborns

Purulent conjunctivitis, Gonococcemia , Septic arthritis

*fever, migratory arthralgias, suppurated arthritis, pustular rash on erythematous areas (not head and trunk) 

N gonorrhea

Treatment & resistance

Treatment

1. 3^rd generation cephalosporin (CEFTRIAXONE!!)(+ doxycycline for co-infection with Chlamydia)

2. fluoroquinolone + doxycycline

3. Neonates: erythromycin eye drops (prophylactically); ceftriaxone if conjunctivitis developed

RESISTANCE

Plasmid: *temM gene – protects from tetracycline

Chromosomal: mtr locus – efflux pump (removes antibiotics)

*penA locus – mutation that alters PBP2 (reduced affinity for penicillin)

*gyrA, gyrB – makes DNA gyrase resistance to ciprofloxacin 

N meningitidis

basic properties

Basic

*Gram (-)

*Diplococcus (kidney/coffee bean shaped)

*Non-motile

*Facultative anaerobe

Location

*Infection begins in nasopharynx (can be asymptomatic)

*Upon entering blood stream, can enter CNS

N meningitidis

Virulence factors

Structural

1. Capsule:(B, C, Y most common in Americas and Europe)

2. Pili: adherence (important for pathogenesis)

3. PorB: interferes with degranulation of neutrophils 

Enzymes

1. IgA₁ Protease: cleaves IgA; allows transmission through mucous membrane

2. Iron sequestering proteins

Toxin

LOS endotoxin: contains lipid A – endotoxin activity

N meningitidis

Lab dx

1. Oxidase (+)

2. Catalase (+)

3. Produces acid by metabolizing both glucose and maltose

4. Must grow on selective media (TM VCN – vancomycin, colistin, nystatin) and non-selective media (Chocolate Agar)

5. Present in large numbers in CSF, blood, sputum

1. Capsular antigen tests not sensitive, infrequently used for ID

N meningitidis

clinical presentation

1. Asymptomatic carriage in the nasopharynx

Meningitis

1. Abrupt headache, fever, meningeal signs:

Brudzinski sign: cervical rigidity

Kernig sign: hamstring spasm

2. Can have petechial rash (but more characteristic of meningococcemia)

Meningococcemia (septicemia)

1. Petechial skin lesions (<3mm, no blanching)

2. DIC (disseminated intravascular coagulation) – with shock

3. Waterhouse-Friderichsen syndrome – bilateral adrenal gland destruction (hemorrhage)

4. Fevers, Chills, Malaise, Headache

N meningitidis

treatment & prevention

Treatment

1. Penicillin (drug of choice)

2. If penicillin contraindicated (e.g., allergies):

a. 3^rd generation cephalosporin(ceftriaxone)

b. chloramphenicol

Prevention

1. Vaccine (only against A, C, Y, W-135 capsular antigens)

2. Prophylaxis (ceftriaxone, rifampin)

Borrelia recurrentis

Basic presentation

Basic

*Gram (-)

*Corckscrew

*MOTILE (6 axial filaments; periplasmic)

*Microaerophilic

*7-20 periplasmic flagella

Location

Varies

Borrelia recurrentis

Virulence factors

Structural

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

B recurrentis

Lab dx

Diagnosis

1. Dark-field microscopy of blood sample (febrile period)

2. Culture on Kelly’s medium (difficult)

3. Stain with analine dyes (Giemsa or Wright)

4. Antibody detection by indirect immune-fluorescence assay (IFA)

B recurrentis

clinical presentation

Infection

Relapsing fever

1. Incubation (3-10 days): chills, fever, headache, muscle aches, shock, convulsions; spirochetes present in blood 

2. Afebrile period (5-6 days): no organism in blood; fever subsides 

3. Relapse (3-10 days): second fever [up to 3-10 recurrences with decreasing severity)

1. Splenomegaly, Hepatomegaly

2. Macular rash

3. Jaundice, CNS involvement, fatality

B recurrentis

Treatment & prevention

Treatment

1. Tetracycline 

2. If tetracyclines contraindicated, use Erythromycin

NOTE: antibiotics administered during AFEBRILE period to avoid JARISCH-HERXHEIMER-type reaction

Prevention

1. No vaccine available

2. Avoid exposure to ticks and lice

3. Rodent control 

Borrelia burgdorferi

basic properties

*largest of spirochetes

*linear genome with multiple linear and circular plasmids

Location

Varies 

Borrelia burgdorferi

virulence factors

Structural

Genome contains linear chromosome with multiple linear and circular plasmids

Can survive without iron (uses manganese)

B burgdorferi

Clinical presentation

Infections

Lyme Disease

Early localized stage (stage 1): Erythema chronicum migrans(EMC)

Early disseminated stage (stage 2):   1. Multiple smaller ECM

2. Systemic signs: fatigue, headache, fever, malaise

3. Cardiac: myopericarditis, CHF

3. Neurologic: aseptic meningitis, facial palsies (Bell’s palsy), peripheral neuropathy     4. Arthralgia  5. Nephritis

Late stage (stage 3)  1. Chronic arthritis  2. Encephalopathy

B burgdorferi

lab dx

Clinical criteria

a. ECM

b. At least one late manifestation: musculoskeletal, nervous, cardiovascular involvement and lab confirmation

Lab criteria (at least one)

1. isolation of Borrelia burgdorferi

2. ELISA or IFA for IgM or IgG antibodies followed by Western blot

- grows well on Kelly’s medium

- stains well with analine dyes (Giemsa or Wright)

B burgdorferi

Treatment

Stage 1

1. Amoxicillin  2. Doxycycline  3. Cefuroxime (2^nd generation cephalosporin)

Stage 2,3

Increased intensity 

Recurrent arthritis, neurological and musculoskeletal diseases:

Penicillin G, cetriazone, cefotaxime

Prevention

2. Wear tight clothing, avoid animal exposure, insect repellant

3. Promptly remove tick (takes long time to transmit spirochete)

Leptospirra interrogans

basic properties

Basic

Spirochete

*OBLIGATE AEROBE

*protoplasmic flagella

*terminal HOOKS

*Very small

Location

Varies

L interrogans

Virulence factors

Structural

Hooks – allows bacteria to burrow into tissue

L interrogans

lab dx

Diagnosis

1. Culture blood/CSF (first 7-10 days) or urine (after 10 days)  in broth or agar medium

2. Dark-field microscopy (blood)

3. Giemsa stain (thick smear) or silver stain

4. Microscopic agglutination test (MAT) – patient serum agglutinates live leptospires [or ELISA]

5. PCR – nucleic acid probes to detect bacterial DNA in serum, CSF, urine 

*whole blood or urine cultures (Fletcher’s medium) – too long

L interrogans

Clinical presentation

1. Either sub-clinical infection, a mild influenza-like febrile illness with myalgia.

Can remit or progress to:

2. Severe systemic infections (Weill’s Disease) with fever, jaundice, renal and hepatic failure, vasculitis, myocarditis, meningitis, and death

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 

Leptospira interrogans

Treatment & prevention

Treatment

1. Penicillin G + Doxycycline (IV)

2. Tetracycline for renal infections

*doxycycline prophylactic in patients exposed to infected animals or water contaminated with urine

Prevention

1. Prevent exposure to matter contaminated with animal urine

2. Reduce contamination by rodent control

3. Vaccinate livestock and pets [distemper-hepatitis-leptospirosis vaccine]

4. Difficult to control completely due to widespread presence in wild

Treponema pallidum

(syphilis)

Basic properties

Gram neg, corkscrew (spirochete)

Location:

usually genital areas

Treponema pallidum

(syphilis)

lab diagnosis

1. Cutaneous lesions examined by dark-field microscopy, immunofluorescence, ELISA, silver stain

2. Serologic tests for syphilis (STS)

A. Venereal Disease Research Lab (VDRL)– maximum sensitivity in secondary syphilis

B. Rapid Plasma Reagin (RPR) (tests for Wasserman antibody)

3. Treponemal tests – confirmatory test 

A. FTA-ABS   B. TP-PA    C. Enzyme immune assay

Treponema pallidum

(syphilis)

Primary – VERY TRANSMISSIVE:   Chancre

*syphilis disseminated in lymphatics, blood, various organs long before appearance of chancre 

Secondary (2-12 wks after chancre)– VERY TRANSMISSIVE

*Alopecia, Fever, weight loss, Lymphadenopathy, Erythematous bilateral rash (palms and soles), Condyloma latum – painless wart-like lesions – packed with spirochetes = CONTAGIOUS

*mucous pouches in mouth, vagina, anus, lesions in bone, liver kidneys

*constitutional symptoms (malaise, fever, etc.) 

Latent (1-40 yrs) – RARELY TRANSMISSIVE (congenital)

CSF exam must be negative to be considered latent 

Tertiary – NOT TRANSMISSIVE, rare congenital

*Gummas of skin and bone, Cardiovascularsyphilis, , Neurosyphilis

Treponema pallidum

(syphilis)

Treatment & Prevention

Treatment

1. Benzathine penicillin for primary, secondary, early latent syphilis 

2. Pencillin G for congenital and late syphilis 

(if penicillin 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:  Avoid sexual contact with infected individuals

Mycoplasma pneumoniae

basic properties

Basic

*No Gram stain (no cell wall!)

*Mulberry-shaped (other Mycoplasma: fried egg look)

*Motile

*OBLIGATE AEROBE

Location

Upper respiratory tract

M pneumoniae

Virulence factors

Structural

1. P1 protein: adhesion factor that destroys cilia of epithelial cells of respiratory tract

2. Sterols in cell membrane: require host cholesterol for membrane formation

Metabolic Products

1. Hydrogen Peroxide: H₂O₂

2. Superoxide: O₂∙

3. Catalase inhibitor

M pneumoniae

Lab diagnosis

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

2. Cold agglutinins: IgM against M. pneumoniae cause RBC agglutination at low temperatures – poor sensitivity, specificity 

3. Complement fixation titer (CF): Ab titer against glycolipid antigens (peak: 4-6 weeks, last years) – poor 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

M pneumoniae

Clinical presentation

Infections

1. Tracheobronchitis

2. Walking pneumonia (ATYPICAL PNEUMONIA) – fever with dry, non-productive hacking cough (some white sputum)

3. Immunopathogenesis: causes polyclonal T-cell response (“superantigenic response)

M pneumoniae

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 

R ricketsii

Basic properties

Basic

*weakly Gram (-)

*non-motile

*rod-coccoid shape

*OBLIGATE INTRACELLULAR (need ATP)

Location

Varies

R ricketsii

Lab dx

1. Micro-immuno-fluorescence (MIF): current standard (need PCR or Western blot to distinguish species)

2. Weil-Felix test: insensitive, low specificity (cross reaction with Proteus); OX-19 (+), OX-2 (+)

3. Culture: Require BSL-3 conditions

R ricketsii

Clinical presentation

Rocky Mountain Spotted Fever

1. Fever: 4-10 days after tick bite

2. Severe headache, muscle pain, lymphadenopathy

3. Rash spreads from extremities to trunk +/- soles and palms

4. Replication in endothelial cells -> vascular damage

5. Rare inoculation eschar

6. encephalitis – leakage from blood vessels of brain

R ricketsii

Treatment

1. Doxycycline

2. Chloramphenicol

Ricketsia prowazekii

Basic properties

Basic

*weakly Gram (-)

*non-motile

*rod-coccoid shape

*OBLIGATE INTRACELLULAR (need ATP)

Location

Varies

R prowazekii

lab diagnosis

1. Micro-immuno-fluorescence (MIF): current standard (need PCR or Western blot to distinguish species)

2. Weil-Felix test: insensitive, low specificity (cross reaction with Proteus); OX-19 (+) 

R prowazekii

Clinical symptoms

Epidemic typhus

1. Incubation (10-14 days)

2. Abrupt onset fever and headache

3. Rash, spares palms, soles, face

4. Delirium, stupor

5. Gangrene of hands or feet (because of increased risk of clotting)

Bill-Zinsser Disease

1. Reactivation of Rickettsia

2. Mild symptoms

3. NO rash

R prowazekii

treatment

Tetracycline 

Doxycycline

Basic

*weakly Gram (-)

*Rod shaped

*NO CELL WALL

* OBLIGATE INTRACELLULAR (need ATP)

Location

Infects columnar mucosal epithelium (compared to endothelial preference of Rickettsiae)

Chlamydia trachomatis

Mechanism of replication

1. Attachment of elementary body (EB) – infectious, metabolically inactive

2. Upon ingestion [phagocytosis or endocytosis] , there is reorganization into a reticulate body (RB) – noninfectious, metabolically active, becomes inclusion

3. Inclusion body undergoes binary fission

4. There is increased growth and RNA/DNA synthesis (requires host ATP)

5. Elementary bodies (from dividing RB) are liberated via lysis (mediated by protease and intracellular Ca²⁺)

C trachomatis

virulence factors

LPS – all Chlamydiae have group specific LPS antigen

MOMP – unique for each species (serovars)

*Resistant to lysozyme (lack peptidoglycan and muramic acid)

*Prevents phagosome-lysosome fusion

C trachomatis

lab diagnosis

1. Molecular amplification tests most sensitive and specific tests available

2. Culture: chick yolk sacs; McCoy cells (specific, but insensitive)

3. Antigen tests (DFA, ELISA) – relatively insensitive

*cell culture with specific stains (Giemsa, iodine staining of glycogen inclusions

C trachomatis

clinical presentation

Serovar A-C:  Trachoma: chronic infection -> corneal scarring and blindness (Africa) 

Serovar D-K: urethritis/PID, ectopic pregnancy, neonatal pneumonia, neonatal conjunctivitis, adult conjunctivitis 

Serovar L1-L3:  Lymphogranuloma venereum: papule or ulceration on genitals -> lymph nodes (pus)

Other

2. Reiter’s 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

C trachomatis

treatment

Lymphogranuloma venereum

1. Doxycycline

2. Erythromycin

Ocular/Genital Infections

1. Doxycycline

2. Azithromycin

Newborn conjunctivitis or pneumonia

1. Erythromycin

Chlamydia psittaci

Basic properties

*weakly Gram (-)

*Rod shaped

*NO CELL WALL

* OBLIGATE INTRACELLULAR (need ATP)

Chlamydia psittaci

lab diagnosis

1. Serological: examine blood for elevated titers of antibodies with complement fixation (CF) and immuno fluorescence tests

2. Intracytoplasmic inclusion bodes DO NOT stain with iodine

C psittaci

Clinical presentation

due to inhalation of bird feces

Psittacosis: viral-like, ATYPICAL PNEUMONIA, with fever, dry, non-productive cough

C psittaci

Treatment

1. Doxycycline

2. Erythromycin

Chlamydia pneumoniae

Lab diagnosis

1. Serological: examine blood for elevated titers of antibodies with complement fixation (CF) and immuno fluorescence tests

2. Intracytoplasmic inclusion bodes DO NOT stain with iodine

C pneumoniae

clinical presentation

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

C pneumoniae

treatment

1. doxycycline

2. erythromycin

Mycobacterium tuberculosis

basic properties

*Acid fast

*Thin rods

*Non-motile

Catalse +

Weakly gram +

*OBLIGATE AEROBE

Location: LUNGS

M tuberculosis

virulence factors

 Structural

1. Mycosides – mycolic acid bound to carb. (Lipid-rich cell wall)

A. Cord Factor: only found in virulent strains; may be responsible for TNF release

B. Sulfatides: inhibit phagolysosome fusion

C. Wax D: acts as an adjuvant

2. Iron siderophore(Mycobactin)

3. Facultative intracellular growth: can survive and multiple inside macrophages.

Slow growing due to G/C rich DNA

M tuberculosis

Lab diagnosis

1. Stain with Ziehl-Neelsenor Kinyoun 

2. PPD Skin test

>10mm (normal)

>5mm (immuno-compromised/AIDS)

*(+) does not indicate active disease

*false negative in AIDS, malnourished 

3. QuantiFERON test: tests IFN-γ levels in response to addition of TB antigens (specific – comes up negative in patients with BCG vaccine) 

4. Species-specific molecular probes(direct detection with molecular probes insensitive)

M tuberculosis

Clinical presentation

Primary Tuberculosis

1. Asymptomatic

-CASEOUS GRANULOMAS  (type IV hypersensitivity)

- Can get Ghon foci and complexes (may/may not be visible on chest X-ray)

2. Symptomatic

- large caseous granulomas 

-cavitary lesions (visible on chest X-ray)

Secondary Tuberculosis

Pulmonary tuberculosis, Pleural, pericardial infection, Lymph node infection, Kidney, Skeletal, Joints, CNS

Miliary TB (tiny tubercles disseminated throughout body)

M tuberculosis

treatment & prevention

RIPES:

1. Rifampin

2. Isoniazid

3. Pyrazinamide

4. Ethambutol

5. Streptomycin

Prevention

Active surveillance, Prophylactic/Therapeutic intervention, BCG vaccine in endemic regions

Mycobacterium avium

Clinical presentation

Clinically indistinguishable from M. tuberculosis. Common in AIDS patients.

M avium

treatment

Treatment

1. Clarithromycin or azithromycin combined with:

2. Ethambutol

3. Rifabutin

*use prophylactic treatment in AIDS patients

Mycobacterium leprae

lab diagnosis

1. Microscopy is sensitive for lepromatous form, NOT tuberculoid form

2. Skin testing (lepromin reactivity) required for tuberculoid form

3. Skin or nerve biopsy: acid fast bacilli (lepromatous) or granulomas (tuberculoid)

*Culture not useful

M leprae

Tuberculoid leprosy

clinical presentation

Increased cellular immune response but decreased humoral antibody response -> granuloma formation -> localized damage to skin and nerves

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

M leprae

Lepromatous leprosy

clinical presentation

Increased antibody response, but decreased cellular immune response -> increase bacteria in dermal macrophages and Schwann cells of PNS (more infectious and deadly!)

- Organism found everywhere (organ, blood)

- 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

*many erythematous macules, diffuse nerve involvement, patchy sensory loss

M leprae

treatment

Tuberculoid from (6mo):

1. Rifampin

2. Dapsone

Lepromatous form (12mo):

1. Rifampin

2. Dapsone

3. Clofazimine