Infectious Disease

Colony Cell Features Features
Staph Aureus Gram (+) Cocci in grape cluster 1 u in diameter Small, 28mm Yellowgolden opaque, Beta hemolytic Colonies on blood agar, facultative anaerobic, 37C
Lab Characteristics
Non-motile - Catalase (+) - Coagulase (+) - Dnase (+) -Mannitol (+) Tellurite reduction + (black colonies), Beta Hemolytic Growth, presence of 7.5% NaCl -Sens.Novabiocin
Source & Transmission

Can colonize nose & skin; Not normal Flora; GI & genital tracts; Transmitted by fomites, sneezes, food - EXOTOXINS - Cytoxins alpha, beta, - Enterotoxins - toxin A (foodpoison) - toxin B, entercolitis (superinf) - emesis (vomit) - Toxic ShockS Toxin - exfoliatin
gamma, delta toxins
Virulence Factors (disease causing)

- Beta lactamase pen resistant - Mutatnt penicillin-binding proteins (methicillin resistance) - COAGULASE - Protein A (opsina. Attack bacteria) - Polysaccharide A - Staph. Decomplementation on antigen - Var Enzym (Spread Fact) - lipase, protease, hyaluronidase, Nucldease, DNase (staphylodornase), staphylokinase (break fibrin)
Associated Diseases
Localized Infections: skin infections - Folliculitis (plug hair) - cellulites - Impetigo (vesicular lesion), Furuncle, Scalded Skin Syndrome (Ritters Disease), Toxic epidermal necrolytic TEN disease Systemic Infections: Food poisoning, TTSS, Osteomyelitis, Infective (septic) Arthritis, Acute Bacterial Endocarditis, Post-viral Lobar Pneumonia (empyema), Bactermia and Sepsis Systemic Infection: - Bacteremia & sepsis - Subacute bacterial endocarditis
Host Defenses / Immunity

No long term immunity therefore recurrent infections possible CD4+ T-cells release cytokines Opsonization by IgG, etc
Treatment / Prevention
Methicillin Vancomycin (if MRSA) Bacitracin (topically) Surgical debridement Drainage of wound
Staph. Epidermis
Gram (+) Cocci in cluster 1 u in diameter
Small, 2-8 mm White (opaque), Round, Gamma hemolytic colonies on blood agar (No hemolysis)
- Catalase (+) - Coagulase (-) - Dnase (-) - Mannitol (-) - Gamma Hemolytic Growth in presence of 7.5% NaCl -Sens.Novabiocin Urease (+)
- Colonize human skin & mucus memb - Normal Flora of the skin - May cause disease in immunocompromised patients following trauma,also iatrogenic intro, or by IV needles Spreads by hematogenous route
Betalactamase (pen resistant) Mutant penicillin-binding proteins (methicillin resistance) same as S. Viridans Exopolysaccharide glycocalyx (SLIME LAYER) sticks to heart Multiple drug resistance
- No immunity against previous infection - Intact skin is important defense - CD4 + TCells release cytokines Opsonizat IgG, No immunity against previous infection CD4+ T-Cells release cytokines Opsinization by IgG
Vancomycin (organism is resistant to most others)
Staph. Saprophyticus
Gram (+) Cocci in cluster 1 u in diameter
Small, 28mm; white (opaque), but older colonies maybe yellowish, round Gamma hemolytic
- Catalase (+) - Coagulase (-) - Dnase (-) - Mannitol Var Depending on strain, Growth in presence of 7.5% NaCl - Resistant to Novabiocin, - Urease (+)
Colonizes human genitourinary, skin (urogenitory) tract, Mucous membranes (lesser extent, GI) Inf. due to poor hygiene & sexual activity, especially in young females
Penicillin resistance Hemagglutinins & other cell surface proteins may mediate Attachment to epithelial cells Urease: may mediate host pathogenesis
Urinary Tract Infect. Upper UTI = pyelonephritis Lower UTI = cystitis Pyuria (puss in urine)
TrimethoprimSulfamethoxazole (bactrim)
Cell Features
Strep Pyogenes Group A Gram (+) Cocci in chains 1 u in diameter
Colony Features
Small, graywhite, round Beta hemolytic
Source & Lab Characteristics Transmission

Non-motile Catalase (-) Dnase (+) Beta Hemolytic No growth > 6.5% NaCl Sensitive bacitracin Human skin Mucous membranes of oropharynx (515%) & vaginal tract Transmitted by respiratory droplets from contaminated food
Virulence Factors
* Hyaluronic acid * Hemolysins (SLO & SLS) - Streptolysins O * beta hemolysis RBC, 02 * sens. => rhematic fever AGN - Streptolysins S * stable w/ O2, little to cause disease * Erythrogenic toxin (3) causes red rash, Scarlet fever (use Dick Test) chks toxin level, if red rash, no AB) fever producing (pyrogenic) are superantigens (strep. Pyrogenic exotoxin) * M Protein : antiphagocytic - > 100 different serotypes Essential for pathogenicity - M proteins resemble x-reactive antibodies lead to rheumatic fever - antiphagocytic - adhesion factor * Hyaluronidase degrades hyaluronic acid * Streptokinase: lyse clots (spreading factor) * Nuclease:degrade D/RNA Spreading factor pus viscosity DNase B = streptodornase ( antibody titer indicates recent S. pyogenes infection
Associated Diseases
* Skin infection * Impetigo (streptococcal pyoderma) * Erysipelas : red rash on face (slapped cheek) * Necrotizing fasciitis: flesh eating strep disease. SPREADS! Systemic Infections Pharyngitis (strep throat, tonsillitis) Scarlet fever (scarlatina) infection w/ erythrogenic leads to red sandpaper rash on trunk or strawberry tongue Puerperal fever (child birth fever) uterine infection Poststreptococcal infection sequelae - Acute Glomerulonephritis (AGN): NO viable organisms present, facial edema & smoky urine - Acute Rheumatic Fever (ARF): NO viable organisms present, include migratory arthritis (aseptic), M protein & heart tissue leads to heart damage
Host Defenses & Immunity

Intact skin is defense Cross-reactive AB ==> ARF. Ag-ab complexes ==> AGN. Look presence of antibody to Streptolysin O and streptodornase
Active infection use Penicillin G or erythromycin Bacitracin cream (GAS susceptible, other Strep are not)
Cell Features
Strep agalactiae Group B Gram (+) Cocci in pairs 1 u in diameter
Colony Features
Small, graywhite, round Beta hemolytic
Lab Source & Characteristics Transmission

Non-motile Catalase (-) CAMP test (+) Beta Hemolytic No growth > 6.5% NaCl Resistant bacitracin Hydralize sodium hippurate Human skin Mucous membranes of vagina, male urethra, throat, GI tract Infects newborns during birth (Puerperal fever)
Virulence Factors
Capsule: polysaccharide Type III capsule is composed of sialic acid (serum resistance) Hemolysin
Associated Diseases
Neonatal meningitis (fever, lethargy, & seizures) invades through respiratory tract - Early onset: 0-5 days infection (in utero) - Late onset: 5-90 days Neonatal pneumonia in utero infection Post-partum endometriosis (puerperal fever) Immunocompromised leads to pneumonia, septicemia, prosthetic disease, puerperal sepsis, skin infection Urinary tract infections

IgG to capsule PMN attack strep
Ampilicillin plus aminoglycosides for infants Penicillin G for adults (* pregnant to carry GBS) Vancomycin for Penicillin sensitive patients Vaccine, Pen. G develops protective IgG cross placenta & protect fetus
Cell Colony Features Features

- Strep bovis - Enterococcus faecalis Group D Gram (+) Pairs and chains 1 u in diameter Small, graywhite, round variable hemolytic response

Non-motile Catalase (-) variable hemolysis bile-esculin (black ppt) Enterococcus grows at 6.5% NaCl (+, present) Group D, S Bovis Strep are (-, not present) Does not grow in manitol! Enterococci colonize at the GI tract. Commensals at the genitourinary tract Infection ==> blood (GI to GU tracts) S. Bovis found in GI tract
Virulence Factors
S. Bovis none (killed easily) E. faecalis: high resistant to antibiotics (vancomycin resistance) Adheres to damaged heart valves & urinary tract epithelial cells.
Associated Diseases
Bacteremia: S. bovis invades blood via GI route. E. faecalis becomes bloodborne via urinary tract infection (UTI) or GI route. UTI enterococal inf. Leads to cystitis (lower) or pyelonephritis (upper) Sub-acute endocarditis: from bacteremia. Enterococcus ONLY infects abnormal valves or prostheses. Bilary tract disease & intraabdominal abscesses Colon cancer prone to S. bovis

Ab important and PMN can attack Strep.
Penicillin G for S. bovis, vancomycin for Pen. Sensitive patiens. E. faecalis: use combination of vancomycin & aminoglycoside
Cell Features
Strep pneumoniae (pneumococcus or diplococcus) also part of S. mitis (No Group b/c lack C cell wall antigens NO Lancefield group) Gram (+) Pairs and chains (diplococci) Lancet shaped 1 u in diameter Grows better in C02 (capnophilic) Encapsulated cell Autolysis (amidase activity) Naturally competent
Colony Features
Small, graywhite, round alpha hemolytic Encapsulated colonies (smooth) Nonencpasulated are (rough)
Lab Source & Virulence Factors Characteristics Transmission

Non-motile Catalase (-) alpha hemolytic* (via pneumolysin activity) (+) for bile solubility (10% Na desoxycholate) Sensitive for optochin (ethyl hydrocupreine) induce lysis of S. pneumoniae (+) for inulin fermentation Inf. Indicate excess # of alpha hemolytic colonies on blood agar plates w/ neomycin. Quellung Neufield Rxn (swelling) Colonizes human upper respiratory tract (commensal) People susceptible to viral infection, allergy malnutrition, alcoholism, debilitation, ciliary motion ==> aspirate into lungs Sickle cell anemia disease Age related Spread by droplet nuclei Capsule (Specific Soluble substance) 80 serotypes Identified w/ Capsule swelling Quellung rxn Capsule protects phagocytosis Non-encap. strains avirulent. C reactive protein (CRP) and used as indicator inflam response as a marker F antigen: part of C carbohydrate, hide capsule Ag are only exposed in nonencapsulated pneumococci Pneumolysin similar to Streptolysin O, Listeriolysin O, & Tetanolysin (found in S. Pyogenes, Listeria, C. Tetani) fxn to inhibit ciliary movemt, bactericidal actv PMN, inhibit lymphocytic prolif. Neuraminadase remove sugar from host glycoprot Peptide permeases: adherence to host tissue IgA protease: cleaves Iga (blocks opsonization surface) - Adhesins: fibronectin - Autolysin: release toxin, infl - Naturally competent
Associated Diseases
Lobar Pneumonia *: in adults & sickle cell anemia patients. Symptoms: - fever, productive cough, dull chest percussion, Xray dxn. Maybe fatal Diagnosis: - Large # of strep & PMN in sputm. Often sequela to viral infection, alcoholism, & smoking (all disrupt fxn of cilia) Meningitis *: in adults. Results from bacterimia, sinusitis, or otitis media, skull fracture, other injury. Symptoms: - fever, stiff neck, headache, maybe fatal Diagnosis: -lumbar puncture,culture Sinusitis *: Often sequela of allergy, or viral infect prevents drainage Otitis media *: Often sequela of allergy, viral infection prevents Eustachian clearance Bacteremia (30% in pneumonias) & 80% in Menigitis *common causative agent

Antibodies against capsule offer typespecific resistance Pneumolysin in high concentration leads to activation of complement
Multivalent, 23 most common capsular ag vaccine confers immunity for a few years Penicillin G (sulfonamides) Vancomycin for penicillin sensitive indv, but vancomycin NOT effective for meningitis b/c doesnt penetrate the BBB (vancomysin doesnt work w/ meninges)
alpha hemolytic: partial breakdown of RBC,
Test Bile soluble Optochin
S. Pneumonoccus Cell lyses Cell lyses
* can be beta hemolytic if grown anaerobically but usually considered as alpha hemolytic Viridans Strep. Not sensitive (resistant) Not sensitive (resistant)
Cell Features
Viridans Streptococci Group includes S. Mutans, S. Mitis, S. Salivarius, S. Sanguis (No Group b/c lack C cell wall antigens NO Lancefield group) Gram (+) Pairs or chains 1 u in diameter
Colony Features
Small, graywhite, round alpha hemolytic
Lab Source & Virulence Factors Characteristics Transmission

Non-motile Catalase (-) does not produce peroxide alpha hemolytic (-) for bile solubility & resistant to optochin (-) for inulin fermentation No group carbohydrate Media grown on sugar produce glycocalyx composed of dextran Organisms are normal flora of oropharynx (commensal) Infection caused by bacteremia following dental work. Can be present in GU tract and can lead to UTI Dextran Glycocalyc (exopolysaccharide): adherence to defective heart valves, block penetration of antibiotics. Forms via GLUCOSE metabolism Lipoteichoic acid: mediates adhesion to fibronectin in blood clots on defective heart valves Glucan polysaccharide : produced by S. Mutans from SUCROSE in mouth thereby allowing attachment of bacteria to tooth enamel. Acids (lactic acid)
Associated Diseases
Subacute bacterial endocarditis common causative agent, from dental work & bacteremia. Infects heart valves & prosthetic devices Dental caries (tooth decay) due to S. Mutans which are localized by large amounts of acid by fermentation of sugars in the mouth. Flourine in water prevents adhesion.

Bacteria killed by host immune system (antibodies & complement) Patients w/ heart conditions are at risk of complications
Penicillin G and aminoglycoside before dental surgery w/ patients w/ heart conditions. Vancomycin for patients allergic to penicillin.
Normal & Damaged Acute Endocarditis - S. Aureus
Abnormal & Damaged Subacute Endocarditis - S. Epidermis - S. Bovis - Enterococcus faecalis - viridans
Cell Features
Bacillus Anthracis Gram (+) Rod, boxcar shaped Pairs or chains NONMOTILE Aerobic Endospores (ex. from soil) Spores resistant to heat, chemicals, dryness, UV, spore coat contains dipocolinic acid & Ca++, low water content 10 x 3 u in diameter
Colony Features
Large, graywhite, flat, waxy, erose colonies on blood agar medusa head colonies rough w/ irregular edges NONHEMOLYTIC Capsule induced in presence of 5% CO2 ==> colonies appear moist
Source & Virulence Factors Lab Characteristics Transmission

Catalase (+) Non-hemolytic, NON-MOTILE can stain polypeptide capsule w/ methylene blue Organism (spores) normally found in soil. Reservoir for spores are herbivores, contaminated animal hides & dust-laden, spore-laden articles. Transmission occurs when host contacts infected animals / products, inhales or eats spores. Spores can also enter via skin wounds or abrasion. ZOONOTIC infection associated w/ cattle Capsule: POLYPEPTIDE composed of DGLUTAMATE (NOT polysaccharide!) Capsule is anti-phagocytic Anthrax toxin: plasmid encoded, comprised of 3 different peptides - Edema factor (EF), impairs phagocytic ability (swelling) - Lethal factor (LF), pulmonary edema is cytolytic for macrophages. Stimulate production of cytokines Skin turns black! Zn metalloprotease, cytokines - Protective Antigen (PA) Cellular uptake processed by host protease to bind to EF or LF ==> allows the factor EF or LF to be internalized by host cell by endocytosis. PA is antigenic LF and EF need PA to be toxic B. anthracis has PA + LF or PA +EF is NOT as virulent as EF + LF + PA. Leads to vascular permeability & neurotoxicity. No PA, then virulent, no damage. Endospore formation: ensures survival of bacteria in harsh conditions. Spore germination requires O2
Associated Diseases
Cutaneous Anthrax: round necrotic black ulcer (ESCHAR) on skin, painless. Toxin is released & blocks capillaries, if untreated leads to bacteremia (grows in blood stream) & cause blood to thicken. Can be fatal if untreated in 4 days. Replicates in blood! Septicemia: B. Anthracis septicemia is rare in humans Respiratory anthrax (Woolsorters Disease) pneumonia following inhalation of spores from infected wool, rare, but fatal. Has a latent period > 2 months. Can hide in lung macrophages GI anthrax: ingest of meat contaminated w/ spores. Mortality ~100%

Ab against polypeptide capsule. Ab to PA prevent binding of LF and EF to PA. If no ab, no time for immune response.
Vaccine for humans confers short-lived immunity (require annual boosting) composed of extract from a virulent but NONENCAPSULATED anthracis Antibiotics: - penicillin G - sulfonamides (sensitive patients) - erythromycin - ciprofloxacin & doxycycline (PROMPT treatment!) Immunize all uninfected animal herds!
Cell Features
Bacillus Cereus Large Gram (+) rods in pairs or chains MOTILE Aerobic Endospores centrally located (metacentric)
Colony Features
Large granular colonies on nutrient agar Mesophilic & nutritionally require amino acid supplements

MOTILE AEROBIC Biotyping not used Vegetative cells & spores normally found in soil, dust, decaying organic matter also in rice, meat products Non-invase inf. Occurs when bacteria and/or spores ingested. Spores survive cooking & germinate ==> produce toxin & ingest preformed toxin (food intoxication) Two Enterotoxins: - Necrotic toxin: heat-labile toxin (LT) that stimulates cells adenylate cyclase. Causes diarrhea - Heat-stable enterotoxin (ST) acts by diff. mechanism than LT, leads to vomiting but not to diarrhea Endospore formation: surivival in harsh conditions. Germination requires oxygen Lecithinase (phospholipase C) enzymes active on cell membranes (associated w/ ocular infection) Cereolysin (potent hemolysin) & Necrotic toxin (associated w/ ocular infection)
Associated Diseases
CHINESE RESTAURANT syndrome Emetic Food Poisoning: upper GI disturbance w/ vomiting toxin forms in rice ==> consume reheated rice w/ toxin ==> food poisoning symptoms arise in about 6 hrs after eating toxinladen food. Diarrheal Food Poisoning: lower GI disturbance w/ diarrhea. Toxin forms in meat / vegetables ==> consume reheated foods laden w/ bacteria (& toxin) symptoms arise w/in 24hrs, food inf. May last for 2 days Post-traumatic endophthalmitis (eye infection) leads to edema. Drug abusers are risk, may cause blindness IV catheter & CNS shunt inf & endocarditis w/ drug abusers, also pneumonitis, bacteremia, meningitis in immunocompromised

Unknown
Fluid & electrolyte replacement if necessary. No other medication. Vancomycin for eye infections. Multiple drug resistance
Cell Features
Corynebacterium Diphtheriae Slender Gram (+) Club shaped pleomorphic rods 1.6 u long x 0.5 u wide usually in L or V shaped Chinese letter clumps (palisades) Cells contain metachromatic phosphatecontaining, inclusion body for energy storage VOLUTIN granules which are lost when cultured in vitro. Non-motile, aerobic
Colony Features
Pleomorphic on SERUMTELLURITE Agar (blackgray colonies indicate tellurite reduction), the differences are NOT correlated w/ pathogenicity C. Diphtheriae - gravis: large black colonies - mitis: small black colonies - intermedius: large gray colonies C. Diphtheriae is very sensitive to sunlight, soaps, desiccation, & antibiotics

Loefflers coagulated blood serum medium, stain w/ methylene blue or toluidine blue to look for metachromatic granules, Catalase (+) Tellurite reduction Iron requirement In vitro test is ELEK test, test for TOXIN ex. CardioToxin (+) test indicates ab-ag ppt toxin (form precipitin line as in double diffusion / Ouchterlongy assays) In vivo test use guinea pig skin test ==> (-) then no redness Humans are only reservoir for C. diphtheriae. They maybe considered normal skin & upper respiratory tract flora Horizontal transmission occurs by respiratory droplets or via contaminated skin lesions in cutaneous form Diphtheria toxin: strong, slow acting binary toxin (has A:B subunit motif) has tissue specificity (heart, nerves, kidney) acts intracellularly following internalization by pinocytosis Detects for cardiotoxin. Peptide B (shuttle protein) binds to receptor on host cells & aids Peptide A in its transport into cell Peptide A (ADPriboslyating enzyme) ribosylates EF2 & stops protein synthesis in host cells Toxin encoded for by lysogenic phage (beta phage). Synthesis controlled by iron levels in environment; toxin expressed when iron levels low and repressed when iron levels high (repressor contains iron, no repressor when no iron) When iron toxin expressed b/c lyse host cell Mycolic acid: (CHIEF VIRULENCE FACTOR!) similar to cord factor of M. tuberculosis, toxic glycolipid K antigen: adhesion in throat
Associated Diseases
Respiratory diphtheria Non-invasive therefore non-systemic (localized) infection => intoxicat ==> pseudomembrane in throat due to inflame. Response. Pseudomembrane can occur regardless of whether strain is toxigenic or not Intoxication: systemic effects of toxin ==> heart toxicity ==> myocarditis, arrhythmias, kidney damage, neurological toxicity Diagnosis must be fast and is based on clinical symptoms. Toxin-cell interaction irreversible & antibodies are ineffective once toxin is bound Start to see endocarditis w/ non-toxigenic strains Cutaneous diphtheria infects open wounds Gray pseudomembrane on non-healing wounds Schick skin test test for protective antibodies (-) test: when diluate toxin is injected , no redness on skin (+) test: redness lack immunity

Peptide B may develop in patient, but development maybe slow DT toxin too small in amount to be antigenic in natural infection
Vaccine consist of formalininactivated (TOXOID) is given as part of DPT vaccine to children. Booster to confer longterm protection 10 years Serum sickness used to test hypersensitivity , too many doses Penicillin G used to kill organism. Erythromycin is a substitute Diphtheroids refers to all NONpathogenic Corynebacteria. Facultative anaerobes. They are opportunistic Elek test to diff. diphtheroids from toxinproducing C. diphtheriae Anerobic Corynebacteria (propionbacterium)
Description
Coryne-bacterium Minutissimum (Foot Associated diphtheroid!) Bacteria produce porphyrins, coral red pigment Organism grows on skin areas with high moisture (ex. skin folds) Superificial infection w/ this organism ==> ex. Athletes Foot w/ scaly plaques especially btw toes. Not pus forming and is called ERYTHRASMA
Diagnosis of erythrasma is based on clinical picture. Lesions when observed under UV (365nm), Woods light appear pinkish to coral red color Non-invasive and treated with oral erythromycin
Cell Features
Listeria monocytogenes - Gram (+) - coccobcilli or short rod (pleomorphic) usually in clumps or short chains Aerobic Tumbling motility 22C & non-motile @ 37C Facultative INTRACELLULAR! No spores!
Colony Features
Pleomorphic & translucent on blood agar Small zone of beta hemolysis Cold storage 4C on bloodcontaining media helps to enrich for Listeria
Lab Characteristics
Catalase (+) B hemolysis (+) Tumbling motility 22C
Source & Virulence Factors Transmission

Organism found in dust, soil, water, sewage, unpasteurized milk, poultry, & vegetables Widespread among animals & humans in GI tract, female genital tract & throat. Vertical transmission: transplacental or during birth Zoonotic transmission: animal contact or ingestion of contaminated foods Activation in carriers who become immunocompromised Listeria infects macrophages & epithelial cells Listeriolysin O (LLO)!!!!!!: mediates escape of organism from phagosome. Found in S. Pneumonia Membranolytic activity is enhanced by low pH & low iron (phagosome bacteria) Toxin is hemolytic (leads to hemolysis) Similar to Streptolysin O (pneumolysin & tetanolysin) Lyse vacuole membranes of macrophage, monocyte and epithelial cells Actin tail: acquires a tail made of actin filaments directs the bacteria ==> cell surface to infect neighborhood cells. Ability to remove iron from hosts transferrin Produce zinc-dependent phospholipase C used to lyse membranes (works w/ LLO)
Associated Diseases
Abortions: pregnant women (due to cell mediated immunity) are prone to listeriosis. (Spont. Abortions!) Neonatal listeriosis: cross in utero to fetus prior to birth. Early onset: 1-2 days after birth, most common form is pneumonia & sepsis ==> lead to granulomatosis infantiseptica: neonatal granulomas and abscesses of skin, eyes, brain. Inf. Occur in utero maybe fatal if not treated Late onset: 5-90 days post-partum, meningitis / meningoencephalitis similar to S. agalactiae Immuno-compromised meningitis: elderly, cancer patients, & renal transplant patients (on systemic steroid treatments). Leading cause of meningitis among this population. CSF PMN Glucose, cloudy culture Food poisoning unpasteurized milk, turkey

T Cellmediated immunity combats intracellular listeria. Listeria induces infected macrophages to secrete IL-12 which promotes T Cells to differentiate to TH-1. TH-1 cells produce IL-2 & gamma interferon. Gamma IFN may activate listericidal fxn in macrophage.
Keep pregnant females away from listeriosis patients. Tetracycline is a drug of choice, or erythromycin Pen G or ampicillin kills organism Ampicilin & gentamycin for neonatal meningitis Pasterurized milk
Cell Features
Clostridium botulinum Large Gram(+) rod Pairs or chains Endospores formed (subterminal location) under poor growth conditions Found in soil, not in patients Spores resistant to boiling for several hr Obligate anaerobic Non-motile
Colony Features
Not usually cultured

Organism not usually grown b/c dangerous. Most labs can not detect toxin Spore stain useful Spores normally found in soil, dust and in decaying organic matter. Vacuum-packed canned goods, the spores may germinate & produce toxin. Food intoxication * Inadequate canning, pH < 7, smoked fish, canned tuna Infant botulism associated w/ honey loaded w/ spores & wound infection ==> subsequent toxin poisoning Botulinum toxin: MOST TOXIC COMPOUNDS known. Eight immunologically diff. toxins produced Types A, B, & E are most commonly causing human disease. Toxins are pre-formed in food. Labile at 121 C at 15 min or boiling food for 20 min (heat sensitive) Toxins are secreted, released by cell autolysis. Botulinum toxin acts as a neurotoxin. It blocks the release of acetylocholine neurotransmitter from poisoned neurons at myoneural junctures. W/in 36hrs flaccid paralysis (Botox for cosmetic purposes) Blocks AcH w/ infants! Endospores formation: survivial in harsh conditions
Associated Diseases
Botulunum food poisoning (INTOXICATION) Early symptoms: vomiting, nausea but no fever. Diplopia (double vision), dysphagia (difficult swallowing), & dysphonia (thickness speech) Late symptoms: flaccid paralysis, respiratory distress ==> can be fatal Infant botulism (INFECTION): infects infants GI tract & produce toxin. Toxin is most common source of spores. Symptoms: weakness, feeble cry, paralysis, respiratory distress. Maybe fatal, could be cause of SIDS. FLOPPY BABY SYNDROME (limp baby syndrome) Honey may contain spores! Wound Botulism: entrance of endospores into wounds ==> germinate ==> toxin

Immunity to reinfection is type specific & permanent
Anti-toxin needs to be given early enough to neutralize toxin monitor hypersensitivity rxn Respiratory support Surgical debridement of wounds & metronidazole for infection Guanidine HCl treatment stimulates acetylcholine release
Cell Features
Clostridium difficile Large Gram(+) rod Obligate anaerobic Sporeformers motile Anaerobic
Colony Features
Not usually cultured
Lab Characteristics
Toxins A & B are detected by lethal effect on cell cultures (within 24hrs) Toxin detected by a) Latex agglutination b) ELISA kit detect toxins A&B
Source & Virulence Factors Transmission

C. difficile is part of normal flora of 10% humans ( in hospitalized) 75% of neonates colonized & serve as reservoirs to others in hospital & at home NEONATES are asymptomatic Nosocomial spread in adults is activation in carrier via changed bacterial balance associated w/ antibiotic use Exotoxins A and B (==> hemorrhagic necrosis) Toxin A: enterotoxin causes diarrhea & colitis (hemorrhagic necrosis). Cause infl. Damage to host tissues Toxin B: cytotxin lethal to cultured cells. Depolymerizes host actin altering host cell cytoskeleton ==> cell loses shape ==> necrosis Endospore formation
Associated Diseases
ANTIBIOTIC ASSOCIATED COLITIS (AAC), ULCERATIVE COLITIS Most common agent; occurs in GI tract pseudomembranous colitis, arises few days after antibiotic treatment (clindamycin, ampicillin & cephalosporins) * Explosive, bloody diarrhea, fever & pseudomembrane in colon (detected by endoscopy)

Commensal, no strong host response Need to restore normal flora
Discontinue current antibiotic treatment & substitute quinolone, sulfonamide or aminoglycosides TMP-SMZ. Vancomycin best! Metronidazole less effective
Cell Features
Clostridium perfringens Large Gram(+) rod Anaerobic Sub-terminal spores (spores in soil, not in patients) Non-motile
Colony Features
Double beta hemolysis on blood agar Thioglycolate medium
Lab Characterist ics

Obligate anaerobic Double beta hemolysis (1 ring beta / 1 ring partial) Lecithinase (+) form ppt rings of insoluble diglycerides Need to confirm A & C serotypes Gas gangrene have different causes

Spores normally found in soil, dust & in feces Wound contamination with dirt leads to infection. C. perfringens similar to c. novyi, c. septicum, c. histolyticum, c. bifermentans Large amount of C02 produced w/ necrosis. Spores growth. Restricted blood flow ==> gas gangrene / myonecrosis Organism can also colonize GI tract & female genital tract (leads to septicemia & organ abscess) in immunocompromised by drug &/or other disease Food poisioning (beta toxin)
Virulence Factors
5 different serotypes based on exotoxins produced. All serotypes ==> alpha toxin (lecithinase) Exotoxins - Alpha toxin ==> lecithinase = phospholipase C (converts lecithin in cell membrane to diglyceride & phosphorylcholine) ==> RBC lysis, destroys membranes & mitochondria - beta, epsilon & iota toxins leads to necrosis & lethality (beta toxin ==> w/ pig bel) Spreading factors: - kappa toxin = collagenase (collagen digestion & liquefication, destroy bone, cartilage, & skin, found in extracellular matrix) - mu toxin = hyaluronidase - nu toxin = DNase - delta toxin = hemolysin - lambda toxin = proteinase (degrades gelatin & hemoglobin) - Enterotoxin (heat liable) inhibit fluid absportion from gut associated w/ serotype A food infection. - Neuraminidase - fibrinolysin - theta toxin: heat & O2 labile (sensitive) hemolysin; membranolytic
Associated Diseases
Gas gangrene 80% serotype A. Infection is result of trauma or surgery. Rapid spread, tissue necrosis & systemic intoxication (via blood) Myonecrosis by alpha toxin, gas production due to fermentation of muscle carbohydrates (saccharolytic activity) Anaerobic cellulites similar to gas green limited to fascia (no muscle invasion) Myositos (muscle infection) Food poisoning Enteritis Necroticans (Pig-bel) associated w/ serotype C producing alpha & beta toxin Septicemia & organ abscesses:

Antibodies & other host defenses ineffective. Antitoxin to alpha toxin is ineffective & leads to hypersensitivity. No immunity to reinforcement
Respiratory support Surgical debridement of wounds & metronidazole for infection Refrigerate meats after cooking Maintain sterility of surgical instruments Hyperbaric O2 environment Penicillin & other broad spectrum antibiotics Penicillin G antibiotics (pg 128)
Cell Features
Clostridia Tetani Large Gram(+) rod In pairs or chains Tennis racket or drumstick appearance Endospores located terminally Obligate Anaerobic Motile
Colony Features
Forms transparent colonies on serum agar cultured ANAEROBICAL LY (O2 sensitive)
Lab Characteristics
Culture C. tetani from wound site (anaerobic) but also culture aerobically to check 2ndary bacterial invaders Staph, Strep

Spores are normally found in soil, dust & may be introduced into host via puncture wounds, gunshots, & burns
Virulence Factors
Exotoxins: a) tetanus toxin (tetanospasmin): coded for on plasmid, produced after germination of spores, released (during cell autolysis) as pretoxin & activated by bacterial protease. - Toxin blocks the exocytosis of inhib. Transmitters, Glycine, and GABA. Results in spastic (rigid) paralysis of voluntary muscles due to un-opposed excitation (tetani) of motor neurons LOCK JAW (TRISMUS) for disease Tetanolysin: is a hemolysin serologically related to Streptolysin O (& listeriolysin & pneumolysin). Also these are found S. Pyogenes, S. Pneumoniiae, Listeria Lyses RBC, PMN, macrophages, platelets & fibroblasts. Endospore formation: survives harsh conditions
Associated Diseases
Deep wound infection ==> TETANUS. Spores enter deep wound Spastic paralysis due to unremitting muscle contraction. Diagnosis: organism may cultured anaerobically Difficult swallowing due to LOCK JAW Opisthotonos: arched back & neck Risus sardonicus ==> fascial grimace Respiratory distress: due to tetanus of diaphragm. Resp. arrest Neonatal tetanus ==> infection of umbilical stump. Infant weak Localized tetanus Cephalic tetanus

Ab against toxin develop in host but too late to stop tetanus & death. Recovery does not confer immunity to reinfection
Vaccination with tetanus toxoid (@ 1st, formalininactivated toxin as part of DPT with boosters give long lasting protection) DPT involves 3 injections beginning of 3 months. Once immunity, booster every 5-10 years. Tetanus antitoxinhuman derived ab to the toxin; respiratory support; hyperbaric oxygen Surgical debridement of wounds & metronidazole (kills bacteria) Antibiotics: inhibit bacterial growth toxin production C. tetani is sensitive to pencillin. Pen. Inhibits normal GABA.
Cell Features
Propionibact erium acnes Gram (+) rod sometimes branching Anaerobic (anaerobic diphtheroid) Non-motile Not spore!
Colony Features
Cultured anaerobically
Lab Characteristics
Propionic acid production Indole (+) Contaiminates blood cultures, b/c its on skin

part of normal flora of skin, mouth & eyes grows in acne lesions metabolize skindervived lipids, blocks sebaceous glands cuase acne & other pustular rxn. May enter via wounds.
Virulence Factors
Lipases (Lipophilic)* split off fatty acids from skin lipids. Inhibit other bacteria but can contribute to tissue inflammation Able to enhance hosts immune system to produce a strong acute inflammatory response
Associated Diseases
Acne vulgaris (common acne) Chronic inflammatory infection of hair follicles. Papules, comedones (blackheads), pustules or cysts on face Bacteremia: ==> endocarditis (opportunistic!)

PMN attracted to bacterial substances Complement activiation occurs
Benzyoyl peroxide topical bacteriostatic effect by oxidation of area Trimethoprim for systemic treatment Retinoids (Vit A) for cystic acne
Lipophilic diphtheroid (appeared in the test bank)
Cell Features
Actinomyces Israelii Gram (+) Rods Long chain branch & filamentous Anaerobic (microaerophilic Non-motile Produce exospores (looks like fungus but its a bacteria!) No nucleus
Colony Features
Cultured anaerobically Mold like structures Colony resembles molar like tooth Lesions: forms sulfur granules b/c of yellow color (CaPO4)

Grows on brainheart infusion agar anaerobically. Staining of sulfur granules from pus, sputum, tissue biopsy w/ hematoxilin-eosin (H&E) Immunofluorescence Normal dental flora (in & around teeth & gum margin) & vaginal flora of women Due to poor hygiene, trauma, or bacterial infection. Endogenous activation (immunocompromised host)
Virulence Factors
A. Israelii NOT very virulent & actinomycoses are polymicrobial infections involves Strep. Sanguis, Strep. Mitis, Prevotella, Porphyromonas, Bacteroides, Fusobacterium, Eikenella, & Treponema denticola. Sulfar Granules are yellow bacterial mats (filaments) bound with calcium phosphate
Associated Diseases
Actinomycosis is caused by obligate anaerobes such as A. israelii. Oral actinomycosis (cervical-facial): overgrowth of normal oral flora or soft tissue mass along the jaw. Chronic, suppurative, granulamatous disease (described as punched out mandible bone lesions) Aspirated into lungs: leads to Lung Actinomycosis (Farmers Lung) chest pain, pneumonitis, empyema, hemoptysis, fever, may spread & appear in X-rays Swallowed ==> abdominal disease. Infection ==> appendix, trauma, or performated ulcer Pelvic Actinomycosis: serious infection, caused by chronic IUD (intravenous used drug) use / inflammation associated w/ STD A. bovis: lumpy jaw Actino: dental plaques

Local, acute inflammatory response (no pain in actinomycosis)
Prevention: - Amoxicillin 812 months - tetracycline - preg. Women (erythromycin) - good oral hygiene Treatment: - Surgical debridgement - drainage - Penicillin G
----------------------------------Disease ===> section ----------------------------------A = Actino A.mycosis A.mycetoma Obligate Aerobic Anaerobe intracellular
Cell Features
Nocardia asteroides Nocardia brasiliensis Gram (+) Short rods Long chains Branch & filamentous Aerobic Non-motile Stained w/ modified (nonalochol) acid-fast b/c of mycolic acid 6% In vivo: INTRACELLULAR!
Colony Features
Cultured aerobically on blood agar Smells musty Grows slow Rough surface (may have aerial filaments)

Acid fast stain of sputum or pus for branching, filamentous bacteria. Use modified acid-stain (sulfuric acid) . Considered paritial/weak acid fast Catalase (+) Superoxide dismutase (+) Abundant in soil & cause of opportunistic infections in immunocompromised patients w/ AIDS, corticosteroids. Most common: - Infection initiates via respiratory route (inhale) - Enters by skin trauma w/ foot the usual site of infection
Virulence Factors
Catalase & Superoxide Dismutase enzymes: high levels resist PMNs intracellular oxidative burst. Formation of long filaments ability resist phagocytosis Mycolic acid
Associated Diseases
Nocardiosis (not contagious, but lethal, & may relapse after treatment) Pulmonary abscesses: cavitating lesions in lungs ==> TB, Crhonic lobar pneumonia Sepsis: spreads from lungs via blood to other organs often to CNS ==> brain abscess, skin ==> kidney lesion Actinomycetoma (aerobic actinomycosis): chronic granulomatous infection of subcutaneous tissues. Sinus tracts are formed draining pus to skin surface. Can lead to damaged bone. Foot is the usual site of infection after injury:

Host generates acute inflammatory (pyogenic) response due to PMN phagocytosis. Ab needed for phagocytosis (require cytokine production). Activated CD8+ T cells are toxic to N. asteroides
Caught early: Sulfonamide Or else: 80% fatality TMP-SMZ for propylaxis
Nocardia asteroides pulmonary infections (from environment) and/or actinomycetoma infections of foot
Nocardia brasiliensis major cause of actinomycetoma infections of foot
Cell Features
Mycobacterium tuberculos (Kochs bacillus) Gram (+) Slender rods in long chains & branches Use Acid-Fast stain Waxy surface (lipid composed *mycolic acid fatty acid, very long chain) if waxy layer removed can stain Obligate Aerobe Looks beaded or granular Non-motile Cell wall: N-glycolym. Acid/base resistant * Catalase (+) * INH (+) TB INTRACELLULAR
Colony Features
Aerobically 510% CO2 & grows slowly!!! Grown w/ MuellerHinton agar, JensenLowenstein agar (egg type) or Middelbrook 7H10 serum agar. Simple medium w/ inorganic salts, asparagines & glycerol. Colorless or cream-colored Dry Wrinkled Colonies develop in 4-8 weeks Cord factor (serpentine cords ) Surface Pellicle in liquid culture
Lab Test Character.

Acid fast stain of septum, but TB is resistant. Culture sputum (egg agar) Chest X-ray: Chk calcification of lesion (Ghon complex) PPD: {cell wall} (Purified Protein Derivative) Skin test (Tine or Mantoux), chk in 2-3 days. Chks for delayed hypersensitivity response. ----------------------< 5 mm = (-) resp or < 5 mm = T_s ----------------------5-9mm=try again > 10mm =(+)resp Severe TB can CD4 T-Cell (AIDS) TB colonies prod. large amnts NIACIN only M. tuberculosis!!!!! Nitriate Red. (+) Bactec sys: chks release of 14CO2

Humans are the reservoir Horizontal transfer via respiratory droplets from infected patients. (secondary TB ex. reactivated infection) Infect via fomites Healthy patients contain TB organisms to tubercles (mini lesions in lung w/ macrophages w/ TB organism intracellularly) Resolves into chronic, quiescent infection Spreads through out body if unhealthy patient b/c reactivation of quiescent infection (secondary TB) Cells can airbone M. Bovis can spread TB-like infection in humans
Virulence Factors
Cord factor composed of trehalose dimycolate: Leads to TNF induction by immune cells, kill itself Catalase: is required for isoniazid sensitivity (INH) Protein antigens of outer coat stimulate selfdestructive host hypersensitivity (TDTH mediated) & acquired immunity Sulfatides (multi-acylated trehalose-2-sulfates): inhibit phagosomelysosome fusion similar to cord factor. Wax D (mycoside): used w/ oil & water (adjuvant, enhance vaccine effective in elicit ab response) Lipoarabinomannin: induce TNF alpha from monocytes & macrophages INTRACELLULAR pathogens, ex. chronic inf. M. Tuberculosis survives under acid, basic, & dry conditions but readily killed by heat (pasteurization). Waxy is a protective layer.
Associated Diseases
TB is a pulmonary disease, dissemination occurs by blood STEPS in disease process: 1.Respiratory droplet reaches alveloi: destruct of PMN by TB 2. Alveolar macrophages ingest TB ==> TB multiply intracellularly ==> tubercle formation w/ minor inflam (tubercle undetect by X-ray) ==> hypersens response TDTH. Tubercle is granuloma composed of inf macrophages, epithelioid cells, multincleatd 3.Caseating necrosis (cheesy) ==> hilar lymph n. (spreads via - lymph w/ 2 output) to a) lung (w/oxygenated) - Adequate CMI (TDTH) response ==> get granuloma infect. stays contained b) Spread via bloodstream, to miliary TB kill . Shot-gun pellet, lungs ,kidneys, GI. Inf. Up to 20 yrs, inf reactivates & develops Secondary TB Primary infections: - heal by fibrosis, calcification ----------------------------------------Ghon complexes, calcified legions visible by X-rays - Cavitating: inf. Blood to kidney, bone marrow,brain, GI - Consumption: waste away - Extrapulmonary TB: Potts disease, vertebral osteomyelit (hunch back) SCROFULA = cervical lymph nodes
Host Defenses Immunity

T Cell mediated delayed type hypersensitivity (TDTH) Antibodies ineffective b/c intracellular in macrophage. Macrophage fuse to form Langhans giant cells. Granulomas form w/ epithelioid cells surround central necrosis. Prevention!! Vents, UV lamps, masks & respirators Vaccine: Intradermal, w/ Live attenuated isolate of M. bovis (Bacile of Calmette Guerin strain or BCG stain)
Combination of drugs, lasts up to 12 months. Antibiotic resist. isolates arise in non-compliant Drug therapies: Isoniazid (INH). INH requires catalase activity of TB to be effective. In PPD+ HIV+ INH, liver toxic 1st line drugs: INH, ethambutol, streptomycin, rifampin, paraaminosalicyclic pyrazinamide combinations, 6 months, Vit B6 Alternative: Kanamycin, cycloserine, INH, & Rifampin== MDR TB is difficult to manage. Immunosuppressive drugs reactive primary TB
Secondary Extrapulmonary TB: Potts Disease (vertibal osteomyelitis) - involvement of cervical lympth one is copying AIDS patients are s - SCROFULA = 10% of as AIDS also bC Non-Runyons mycobacteria - M. tuberculosis - M. bovis - M leprae Runyons classification of atypical mycobacteria == > Pigament Formation in <== Group Growth Rate Light Dark Species I II III IV Slow Slow Slow Rapid Cell Features
MOTTS g(+) slender rods long chains, branching waxy surface mycolic acid non-motile aerobic visualize w/ acid-fast
+ + Colony Features
Runyon Groups I-III are cultured aerobically & grow very slowly
+ -
M. kansasii, M. marinum M. scrofulaceum M. avium-intracellulare complex M. fortuitum-chelonei complex Virulence Factors

1. Mott are low virulence 2. produce no catalase 3. protein antigens (killself) 4. survives in macrophages 5. survives in acid/basic, dry 6. MOTT are multi-drug resistant

Acid-fast stain Produce no niacin MOTT species are ubiquitous in nature Cause disease by opportunistic infections No person to person transmission
Associated Diseases
Group I - M. kansasii, pulmon. Inf. - M. marinum, swim pool granuloma Group II - M. scrofulaceum, cause scrofula Group III - M. Avium Intracellulare (MAC) Group IV - less mycolic acid - M. smegmatis (foreskin)

T cell mediated DTHR AB ineffective b/c bacteria are intracellular Granulomas may form w/ MOTT infection
Group I - Kansaii: multidrug + INH - Marinum: rifampin & ethambutol Group II - Scrofulaceum: rifampin Group III - MAC: ethambutol, streptomycin, rifampin Group IV - Smegmatis, amikacin
Cell Features
Mycobacterium Bovis Gram (+) Slender rods in long chainsbranching Waxy surface (mycolic acid) Obligate aerobe Non-motile Acid-fast Catalase (-)
Colony Features
Grows very slowly Colonies develop in 48 weeks Grown on MuellerHinton agar, JensenLowenstein agar or Middlebrook 7H10 serum agar Cord factor (trehalsoe dimycolate) produce pathogenic strains leads serpentine cords& surface pellicle in liquid culture.

Acid fast staining Of sputum Chest X-ray PPD skin test (+) Colonies, colorless NO NIACIN Catalase (-), resistant to isoniazid, INH (differs from TB) Detected by Bactec within 10 days cultivation Mammals are only reservoir b/c under zoonotic. Infection occurs by ingestion of Raw Milk obtained from infected animals. Human to human transmission can occur via respiratory droplets from individuals with secondary TB
Virulence Factors
Cord factor: ( Trehalose dimycolate) gathers M. Bovis Into chains. Catalase (-) ==> INH (-), resistant Proteins antigens of outer surface stimulates selfdestructive host hypersentivity Other factors enable organism to survive in macrophages (INTRACELLUULAR) Waxy layer (mycolic acid w/ trehalose) contributes to bacterias ability to survive under acidic/basic, dry conditions & to resist exposure to many disinfectants. Multiple Drug Resistant (MDR) b/c of the waxy layer or porin size.
Associated Diseases
Causes pulmonary infection, similar to TB Infections: - GI tract - scrofuloderm (skin inf) - osteoarticular TB (joints) Use of immunosuppressive drugs (steroids) re-activate primary M. Bovis. PPD + indicate exposure to M. Tuberculosis or M. Bovis

T Cell Mediated delayed hypersensitivity (TDTH) AB are ineffective b/c intracellular in macrophage Macrophage fuse to form Langhans giant cells. Granulomas form w/ epitheliod surrounding central necrosis
Decontaminate w/ concentrated NaOH Prevent development of drug-resistance, use combo of drugs.
Cell Features
Mycobacterium aviumintracellulare MAC complex Runyon Group III & MOTT Gram (+) Slender, rods, in long chains Aerobic Waxy surf= mycolic acid Non-motile Acid-fast Catalase (-)
Colony Features
Grows very slowly Grown on MuellerHinton agar Middlebrook 7H10 serum agar (w/o pigment production)

Acid fast stain of sputum Catalase (-) Colonies are colorless & do not produce niacin Nitrate Red. (-) Chest X-ray Bactec test: test for C02 production PPD skin test sometimes (+) PPD(-) when immunocompromised patients w/ AIDS MAC species are ubigquitous in nature (soil, dust, & throats) of normal humans & animals MAC can cause disease by OPPORTUNISTIC infections of birds & immunocompromised humans, AIDS patients w/ CD4 T cell.
Virulence Factors
1) MAC are organisms low virulence 2) Do not produce catalase, there INH becomes resistant 3)Protein antigens of outer coat stimulate selfdestructive host hypersensit. 4) Bacterial factors enable organism to survive in macrophages. Therefore, INTRACELLULAR 5) Bacteria survives in acid/basic 6)MAC are naturally multdrug resistant
Associated Diseases
MAC pulmonary inf. common in AIDS patients MAC pulmonary inf. similar to TB PPD(+) may appear (-) b/c suppressed T cell, T_s * Main route of inf. into AIDS patients is the GI tract. MAC residing in macrophages INTRACELLULAR disseminate from lymph nodes to spleen & lungs forming lesions. May spread to all organ systems Tubercle (granuloma) formation in MAC inf. of AIDS patients is NOT observed. Tubercle seen in M. Tuberculosis.

T cell mediated (DTHR). Antibody ineffective b/c bacteria are intracellular
Multi-drug therapy b/c most are multidrug resistant (MDR) 1st line drugs: - ethambutol - streptomycin - rifampin
Catalase (-) M. Bovis M. Leprae M. Avium Intracellulare (MAC) Acinetobacter
Catalase (+) M. Tuberculosis Norcadia
Cell Features
Mycobacterium Leprae Hansens Disease Gram (+) Slender, rods, long chains, & branching Waxy surface mycolic acid Non-motile Aerobe acid-fast stain Catalase (-)
Colony Features
CAN NOT BE CULTURED IN VITRO But inside ARMADILL OS & Foot pads of mice.
Lab Characteristics
Acid-fast stain skin test. Lepromin test: similar to PPD Catalase (-) PCR and rRNA probes Lepromatous form: skin lesion biopsies & nasal secretions, look for acid fast bacilli in macrophage (foam cells) globi Tuberculoid form: difficult to observe bacteria

Humans & armadillos are the only reservoirs Horizontal transfer occurs via respiratory droplets Skin contact (ulcerative lesions) Leprae likes to grow at lower temp. extremities ex. skin
Virulence Factors
1) Phenolic Glycolipid (PGL-1 antioxidant prevent phagocyte 2) LAM: along w/ PGL-1 inhibits T cell proliferation, cause anergy (no responsiveness) 3)Prefers lower temp. limits infection to skin, nasopharynx, & testicles. Leprosy is primarily a skin disease. 4) INTRACELLULAR survival (no pain sensation)
Associated Diseases
Leprosy, lots of symptoms Tuberculoid Leprosy: Borderline (intermediary) Leprosy subdivided to Lepromatous Leprosy. The patients progress of the disease on hosts immune Depends on intensity of CMI (cellular Mediated Immunity) response - Strong CMI: tuberculoid - Impair CMI: lepromatous a) Tuberculoid leprosy: strong CMI, tuberculoid leprosy develop w/o neurological involvement. Disfigured (Lions face) scars Biopsy shows few bacilli b/c few bacteria are in lesions Activated macrophages kill leprae. T cells is detected by lepromin test (+) Lepromatous form not infect b) Intermediary Leprosy c) Lepromatous leprosy: disfigured due to nodules (lepromas), sense loss, pain, & temp. Weak CMI. No TDTH. Biopsy w/ large # of bacilli. Respiratory congestion immune anergy (no activation of macrophages) Numerous T_s cells observed but giant cells & epitheliods are rare. Patient w/o hypers lempromin(-). HIGHLY INFECTIOUS

T cell mediated (delayed type hypersensitivity response) In tuberculoid form (strong CMI) Granulomas form w/ epithelioid cells surrounding central necrosis. Lepromatous form: strong AB response but weak cytokine response.
Multi-drug therapy dapson w/ rifampin or dapson w/ clofazimine (for lepromatous leprosy))
Cell Features
Neisseria gonorrheae G(-) Diplococci Aerobe capnophilic as well Non-motile Lipooligosaccharide (LOS)
Colony Features
Chocolate agar T1-T2: pili T3-T5: no pili
Lab Characteristics
Catalase (+) OXIDASE (+) Contains enyme cytochrome C, turns black, due to oxidation ONLY glucose (+) Maltose (-) Sucrose (-) Lactose (-) Ferments under glucose, NOT (-) Superoxol (+) test (30% H202) Use Thayer-Martin (TM) or (NYC) agar for 48 hrs. TM ==> contains vancomycin inhibt g(+) Colistin inhibit: g(-) rods Nystatin inhibit: yeasts Trimethroprim inhibit: Proteus

Humans ONLY reservoir Horizontal transfer occurs via sexual contact. Complement deficiency (C5-C8) leads to meningitis, predisposes patient to coccemia.
Virulence Factors
Lipooligosaccharide (LOS) similar to LPS (+attract PMN to primary inf site) 1. Cell can add sialic acid to LOS, more C resistant 2. Cell wall frag are released 3. Pili: attach to epithelial cells especially urogenital cells + mucosal surfaces undergoes ANTIGENIC VARIATION 4. IgA protease: prevents IgAmediated opsonization on mucous membranes 5. 3 outer membrane proteins (omp) display antigenic variation - Protein I: Inhibit phagolysomal fusion + promote endocytosis - Protein II: Opacity protein, adhesion. Undergoes antigenic + phase variation. Therefore makes macrophage difficult to kill bacteria - Protein III: Porin protein, complex protein I, binds IgG blocking AB = Rmp, blocks C mediated bactericidal ab f(x) 6. Beta lactamase: plasmid encoded PPNG 7. Fe binding protiens 8. Invasiveness epithelia engulf N. gonorrhea, via INTRACELLULAR 9. Cell wall display toxicity epithelial cells (tracheal cytotoxin of B. pertussis) 10. Autolysis/natural comp. 11. Type IV pili: g(-) twitch, cell specificity + phage abs
Associated Diseases
Male STD Gonorrhea: men are systemic, at the urethral. Leads to urethritis, painful urination or dysurea w/ purulent discharge. Female STD Gonorrhea: inf. vaginal or anal. Endocervical most common. Inf. mostly asymptomatic but vaginal discharge, dysuria + bleeding may occur. Untreated results in salpingitis (Fallopian tubes), cervicitis, and pelvic inflammatory disease (PID). Inf. of liver may cause perihepatitis (FritzHugh-Curtis Syndrome) !!! Neonates: purulent conjunctivitis acquired by newborn during passage via birth canal (Ophthalmia neonatorum) Monoarticular arthritis (single joint): #1 agent of arthritis in young adults. Found in female knees (due to bacteremia) Rash on leg!!! Disseminate Gonococcal Infection (DGI) ==> septicemia ==> LOS ==> toxicity ==> leads to chills skin lesions (rash) ==> spreads to joints ==> endocarditis

N. gonorrhea infection leads to local acute inflammation due to PMN activity & complement activation. No immunity to reinfection possibly b/c of antigenic variation
Ceftriaxone (expensive) Alternative: - Spectinomycin - doxycycline
Cell Features
Neisseria meningitides G(-) Diplococci Aerobe Capnophilic Non-motile Lipooligosacharide (LOS) similar LPS Naturally competent
Colony Features
Grows on chocolate agar, produce transparent colonies

Catalase (+) OXIDASE (+), only glucose & maltose are used by this species Glucose (+) Maltose (+) Sucrose (-) Lactose (-) Needs & uses Fe Humans are the only reservoirs. Heathly individuals may be carriers of N. meningitides. 2-8% of population are carriers but in epidemic year will increase to 40-90%, colonizes the nasopharynx. Horizontal transfer occurs via respir. droplets & requires intimate contact (ass. w/ xchange of respir secretions) Activation of infection in carrier due to depressed immune response. 1. Capsule made of polysac: 13 serogroups A,B,C,W-135, Y provides antigenic variety, encapsulated strains resist phagocyt + facilitate invade B = poorly immunogenic + resembles uropathogenic E. colis. K1 capsule (neonatal meningitis) E. coli ass. w/ neonatal meningitis B capsule rich sialic acid resid. Pili: attach to epithelial (nonciliated) cells. Antigenic variation IgA protease: (similar to gonorrheae) prevent IgA opsonization on mucosal surfaces Beta lactamase: plasmid encoded Iron-binding protein: scavenging Fe from transferin, lactoferrin of host Protein II ONLY!!! = Opacity Protein, involved in adhesion. Undergoes antigenic + phase variation Facultative intracellular pathogen: enter phagocytic vesicles & avoids death. Similar to N. Gonorrhea in non-ciliated mucosal cells Type IV pili: adhesion, twitch motility Intracellular: into m.phage
Associated Diseases
Epidemic meningitis: youngsters & military personnel. * Symptoms: fever, neck pain (stiffness), headache. Diagnosis: from spinal tap. CSF, chk pressure, cloudiness, culture (+), # of PMN & low glucose (confirm septic meningitis) Meningococcemia: upper respiratory infection, result in meningitis. Sepsis is diagnosed by skin rash. Disseminated Intracellular Collapse (DIC) ==> rapidly fatal. Waterhouse-Friderichsen Syndrome!!!: rapid DIC, vascular collapse, shock & death w/in 6-8 hr & adrenal bilateral hemorrhage. FATAL. Meningococcal pneumonia: w/ carriers, pneumonia after viral infection.

Pili available may get activation to complement, results inflammation and pus formation.
Treat as early as possible Penicillin G Alternative: Chloramphenicol Rifampin, given prophylactically VACCINE: polyvalent capsular antigen New vaccine Menactra with capsule conjugated to vaccine.
Not on final!!!
Eikenella corrodens
Cell Features
G(-) Slender rods Faculatative anaerobe Capnophilic LPS Twitching motility
Colony Features
Grows on blood agar that shows pitting of the agar Bleach like odor on agar

Catalase (-) Oxidase (+) No sugar is used (lack oxidative & fermentative) Aerobic growth requires hemin supplementation Lysine decarboxylase (+) Urease (-) Gelatinase (-) Indole (-) Nitrate reduction to nitrite only Yellow pigment production Human mucous membranes (mouth & upper respiratory tract) are reservoirs Normal flora 1. LPS (endotoxin) 2. Pili: attach to epithelial cell 3. Type IV pili: adhesion to host cell surface, twitching
Associated Diseases
1. Human BITE WOUND!!! Could also be mixed infections (staph & strep) Clenched fist. Associated w/ lower extremity infections by stepping something contaminated to break the skin. 2. post-surgical infections: soft tissues w/ abscesses & arthritis, empyema often seen. Spreads throughout body. Associated w/ meningitis, endocarditis, osteomyelitis & soft tissue abscesses

NA
Augmentin (clavulanic & amoxicillin) Alternative: Tetracycline or quinolones
Cell Features
Acinetobacter Baumannii G(-) Coccobacilli Obligate aerobe Non-motile Oxidase (-) Nonhemolytic Glucosa oxidized
Colony Features
Grows on blood agar Produce colonies that are nonhemolytic

Oxidase (-) Does not ferment sugars but glucose oxidized Widely distributed in nature (free living saprophyte) Often associated w/ hospitals Organism is able to survive on moist surfaces & skin Acinetobacter is only 2nd to the nonfermenting Pseudomonas aeruginosa in causing nosocomial infections maybe associated w/ hospital outbreak Ex. Acinetobacter, Xanthomonas, pseudomonas, can colonize mechnical ventilator ==> introduce into respiratory tract of patient undergoing assisted ventilation
Virulence Factors Associated Diseases

1. LPS (endotoxin) 2. drug resistance(s) Acinetobacter species are hospital acquired in warm seasons Post-surgical infections of soft tissue with abscesses is often seen. Organism may be also involved w/ respiratory tract infections and urinary tract infections.

NA
TMP-SMA (Bactrim) similar S. Saprophyticus Alternative: - Kanamycin, - Colistin, - Tetracycline ---------------------Resistant to Penicillin b/c of beta-lactamase
G (-) bacilli
Bordetella pertussis
Cell Features
G(-)
Colony Features
Phase I most virulent grows on Bordet-Gengou (contains potatoe starch, glycerol, & 50% blood) has a pili & O-antigen are expressed
Lab Characteristic
Nasopharyngeal swab ==> incubate 10 days

Humans, the only reservoirs!!!
Virulence Factors
Associated Diseases
3 stages of whooping cough or pertussis (intense cough) 1. Catarrhal stage: Most infectious, most bacteria. Most contagious. RRHEA 2. Paroxymal stage: violent cough, vomit. CNS damage. Less contagious. VIOLENT stage 3. Convalescent stage: gradual reduction in cough, may last 1-6months

Ab made against capsule. Infection is non-invasive w/ bacteria remaining in respiratory tract.
Erythromycin Alternative: Tetracycline chloramphenicol Paroxymal stage: oxygen therapy may be effective & steroids severity. Vaccination: Kills phase I bacteria, DPT vaccine w/ boosters 4,6, 18 months. This vaccine has been replaced by ACELLULAR vaccine w/ reduced side effects. PT, FHA, pertactin, & pili are commonly used.
1. Capsule: A good marker for vaccine effectiveness but ab is Coccobacilli not protective. Horizontal 2. Exotoxin (WHOOPING transmission is Singly or 3. PERTUSSIS TOXIN (PT) is Oxidase (+) COUGH!) by respiratory pairs, chairs heat-labile binary toxin. droplets among Deactivates inhibitory GTP Direct children Obligate binding* proteins (Gi) by ADPfluorescent Ab aerobe ribosylating them test (DFA) HIGHLY Active B (adhesion factor) Produce small CONTAGIOUS NO carbocomposed 5 unique polypeptides pearl-like or ELISA (90% gets hydrate & mediates w/ A subunit, metallic colonies infected) fermentation results in cAMP. Toxin blocks & oxides PMN & inhibits movement by Produce small zone amino acids chemotaxis & activates of hemolysis pancreatic insulin production by Non-motile Islet cells. CO2 help growth Cyclolysin: dual f(x) toxin, Requires: hemolsyin + adenylate cyclase Cell sensitive to nicotinic acid heat, dry, & chem.. 4. Adenylate Cyclase: inhibit cell f(x), especially WBC, edema Blood, helps factor of B. anthracis. neutralize inhibitory Hemolysin: inhibit leukocyte effects of fatty acid, chemotaxis, phago & killing sulfides & H202 5. tracheal cytotoxin: peptidoglycan frag, damages Phase II & II less ciliated cells. Stim IL-1 release virulent. No blood 6. Adhesion factors: pili on phase IV. (fimbriae) display phase variation on/off VIR gene 7. Filamentous Hemagglutinin (FHA) attach to ciliate epithelial Phase variation cells (exp. on/off gene) 8. Pertactin: adhesion factor 9. LPS = endotoxin Lipid A & X, X more potent!!! ** B. bronchispetica: motile, causes cough in dogs, kennel cough, unique-nitrate reduction (+), mild symptoms Phase Description Phase I Pili & O-antigen expressed Phase II & III Bacteria express different antigens, less virulent Phase IV Pili & O-antigen NOT expressed. Avirulent
G (-) bacilli
Haemophilus influenze
Cell Features
G(-) Coccobacilli bipolar stain chains/filam ents facultative anaerobic Capnophilic CO2 Non-motile Naturally competent!!!
Colony Features
Grows on chocolate agar producing small colonies that are non-hemolytic contrast to Beta-Hemolytic: - H. Ducreyi - H. hemolyticus Capsule: Quellung Rxn, destroyed by autolysis by endogenous enzyme Requires: (hexe, navy) - Factor X: HEME - Factor V: NAD grows on chocolate agar H. influenzae recovered during primary isolation on standard blood agar. Also grows in close proximity to S. Aureus (beta hemolytic) Satellite phenomenon: test for nutritional req.
Lab Characteristic
Catalase (+) Fermentation rxn are variable (glucose only) Tryptophanase (+) Nitrates used as terminal electron acceptors Vancomycin sensitive Requires X & V factors and CO2 Specimens: CSF, blood & carry out antigenic typing of capsule (Quellung rxn)

Humans are only reservoir for H. influenzae. Nonencapsulated variants are considered to be normal flora of the pharynx & conjuctiva. Carrier rate is ~30% Hortizontal transmission primarily respiratory droplets Individuals had protective ab to type b capsule by age 5-6 Carriage is mostly by nonencapsulated strains, maybe non-typable encapsulated strains. Lead to localized infections, w/o dissemination
Virulence Factors
1. Capsule: Type b is most commonly associated w/ disease including meningitis (90% caused by strains) Type b capsule is composed of polyribitol phosphate (PRP) Capsules can elicit Quellung rxn (serotyping) 2. IgA protease: prevents opsonization by IgA 3. Beta lactamase: encoded on plasmid, confers resistance to penicillin 4. Pili: adhesion factor, not well characterized 5. LOS
Associated Diseases
Nasopharyngitis: H. influenzae infections (include non-typable or non-encapsulated strains) Infection may become sinusitis, otitis media or cellulites also pneumonia, chronic bronchitis, epiglottitis. May lead to bacteremia & septic arthritis Epiglottitis: inflamed epiglotis swollen, red, edematous tissue leads to airway obstruction Meningitis: H. influenzae (type b) #1 cause of meningitis in young children - 6 Purulent conjunctivitis (pink eye): caused by H. aegypticus (Kochs Weeks bacillus)

Neonate got ab from mother & was protected for first few months of life. Eventually, reproduce its own.
Ceftriaxone or cefotaxime Combination of: Cefotaxime w/ ampicillin Alternative: (sensitive Pen.) chloramphenicol Vaccine: Composed of polyribitol phosphate (PRP) conjugated to protein. Used as a booster
G (-) bacilli
Haemophilus ducreyi
Cell Features
G(-) Coccobacilli bipolar stain facultative anaerobic Non-motile
Colony Features
Grows on blood agar produce small colonies that are hemolytic Requires only heme (Factor X) no need NAD b/c can synthesize
Lab Characteristic
Catalase (+) Glucose is fermented Requires Factor X (heme) Vancomycin resistant

Humans are the only reservoir in genital tracts Hortizontal transmission occurs via sexual contact
Virulence Factors
1. LPS (endotoxin)
Associated Diseases
H. ducreyi causes SOFT chancre (chancroid), painful, gential lesions & lymphadenopathy (enlarged lymph nodes). Enters via break in skin. Can carry to inguinal lymph nodes & multiply. May result in massive swelling. Highly contagious.

na
Erythromycin Alternative: Sulfa drugs (sulfonamide) or streptomycin
Exam Question: What is the causative agent of cahncroid? H. ducreyi
G (-) bacilli
Klebsiella pneumoniae (Friedlanders bacillus)
Cell Features
G(-) Large & long bacilli facultative anaerobic Non-motile
Colony Features
Grows on blood agar produce slimy mucoid colonies b/c of capsule, nonhemolytic. Spreading
Lab Characteristic
Oxidase (-) Slow fermentation of glucose, lactose & sucrose (pink colonies on MacConkey lactose agar) Bile salt selectin Indole (-) Methyl red (-) Voges-Proskauer (+) Citrate (+) Urease (+) H2S (-) Capsule: Quellng Rxn

Widely distributed in nature (soil, vegetables) Often associated w/ nosocomial infections: K. pneumoniae is normal flora of human colon. Nosocomial infections: organism is transmitted by dwelling catheters & endotracheal tubes Mostly in immunocompromised, hospital patients Diabetics risk
Virulence Factors
Capsule: resist phagocytosis, attracts macrophages to area Urease: develop UTI R plasmid: codes for Pen. & aminoglycosid e resistance LPS, endotoxin ST & LT enterotoxin
Associated Diseases
1. Lobar pneumonia & bronchopneumonia: associated w/ hospital acquisition by alcoholics, diabetics, & patients w/ chronic pulmonary disease. Symptoms include: fever, productive cough, empyema, hemoptysis (spit blood) & thick currant jelly sputum. 2. Urinary Tract Infection: common in hospital settings, b/c compromised by surgery, catheters, bladder retention etc 3. Bacteremia caused by Klebsiella & E. Coli in hospital settings. 4. Tropical sprue

Ab made against capsule
Cefotaxime & gentamycin Sensitive Pen: TMP-SMZ (Bactrim)
G (-) bacilli
Legionella Pneumophila
Cell Features
G(-) Catalase (+) Thin rods Seen w/ Ag impregnatio n w/ StarryWarthin procedure Motile Aerobic Grow w/ CO2
Colony Features
Grows very slowly on BCYE (buffered charcoal yeast extract) agar produce small iridescent colonies Colonies have brown pigmentation BCYE +Cysteine + Fe gets L. pneumophila to grow
Lab Characteristic
Catalase (+) Superoxide dismutase (+) Produces brown pigment in vitro Gelatinase (+) Oxidase (+) No fermentation of sugars. Bastards can hide in amoeba difficult to kill, even w/ Chlorine

NO horizontal transmission btw humans to humans (not infectious) Air conditioning tanks, whirlpool baths, humidifiers, hot water systems, shower heads, & contaminated water supply systems Can be found in hospitals & community settings Survives intracellularly in amoebae Transmission occurs by inhalation of aerosols & aspiration of contaminated water * patient w/ immunosuppressive drugs, smoking, or had surgery are at high risk.
Virulence Factors
LPS (endotoxin) Inhibition of fusion of phagosome & lysosome in macrophages & monocytes INTRACELLULAR survival Production by L. pneumophila of proteolytic enzymes: Cytotoxin: blocks PMN oxidative burst Capsule = F1 fraction Phosphatase: blocks superoxide anion production by stimulated PMN Hemolysin (legolysin) MIP gene product (macrophage infectivity potentiator) promotes phagocytosis by binding to a complement factor Beta lactamase
Associated Diseases
1. Legionnaires Disease: Atypical pneumonia. Non-productive cough, classic shallow sound when pertuss lungs in back. Infections may be nosocomial or community acquired (hotels or cruise ship) 2. Pontiac Fever: fever, chills, nausea, & headaches develop w/in 48 hrs after infection (flulike symptoms). Occurs more often in younger patients.

Ab are ineffective against intracellular bacterium. Cell mediated immunity most important & activation of macrophage Acquired immunity obtained (protect against subsequent infection)
Erythomycin or other macrolide antibiotic Cephalosporins & aminoglycosides Prevention: Very hot water flashing! 80C for 30 min or use UV light. Chlorination is not very effective since L. pneumophila survives by colonizing water-dwelling amebae
G (-) bacilli EQ!

Pseudomonas aeruginosa
Cell Features
G(-) Long & thin bacilli in chains or singles Cant carry out fermendation, can use any carbon source oxidatively Opportunist Resistant to many chemical disinfectants Associated w/ resistance to many antibiotics. Produce a biofilm which contributes to antibiotic resistant & ability to grow in presence of disinfectants
Colony Features
Has Bluegreen color & grape-like odor Strong beta hemolysis Many will fluoresce under UV light due to pyoverdin (fluorescein) production
Lab Charact.
Oxidase (+) Catalase (+) No sugar fermentation but glucose is oxidized Triple sugar iron (TSI) (-) Citrate (+) Nitrate red. (+) Fruity (grapelike) odor Pyocyanin production (blue-green pigment) Beta-hemolysis

Widely distributed in nature (soil & water) often associated w/ moist areas in hospitals May be found in swimming pool & whirlpools which are inadequately chlorinated, & raw vegetables Nosocomial infections Found to exist in disinfectant & eyewash solutions.
Virulence Factors
Exotoxin A (diphtheria toxinlike toxin) A subunit has ADPribosyl transferase activity & B subunit binds to cell. Leads to inhibit protein synthesis. Target cell: heart & liver. Exoenzyme S: mediates burn wound inf & lung inf of cystic fibrosis (CF) Hemolysins: disrupt membrane lipids & acts synergistically w/ phospholipase Phospholipase C: disrupts membranes & rhamnolipid (inhibits ciliary action in respiratory Lipases & lecithinases destroys tissue & blood cell, inflam Mucoid ExPoly. (MEP) = alginate, form biofilms:adhere, immbolize organism. Biofilm, resist. to drugs & disinfectants (iodine). Glycocalx resist phagocytosis. Collagenase: degrade collagen Elastase; cleaves IgA, IgG, & complement. Alkaline protease. PYOYANIN: blue-green pigment w/ bacteriocidal activity. Pyoverdine = fluorescein (green-yellow UV) Multiple Antibiotic Resistance: beta-lactamase, acetylating enzymes.
Associated Diseases
1. Necrotizing bronchopneumonia: fever, cough, purulent sputum, & lung abscesses. 2. Burn wound infs: black blue wound, fruity smell spreads into adjacent healthy tissues. #1 problem in burn patients. Use Woods UV to see P. aeruginosa. Seen in post-surgical wound infections. 3. UTI: catheterization 4. Sepsis/bacteremia: septic shock & death. 5. Corneal keratitis: contact lens lead to blindness 6. Otitis externa (swimmers ear): cause otitis media 7. Pseudomonas folliculitis: skin abrasions, unchlorinated hot tubes 8. Osteochondritis: puncture wound of foot. Tennis shoes 9. Podiatrically important infect nail. Eats nail & turn into green goo
Host Defenses Immun.

Immunocompetent patients have Intact skin important to resist this organism. No immunity to reinfection
Multi-drug treatment (Kirby-Bauer test, antibiotic resist. Profile) 1. Gentamycin + azlocillin 2. Augmentin Sensitive Pen: Aztreonam For meningitis: Ceftazidime UTI & Respir. Disease Quinolone Prevent burn wound infect : Daily wound debridgement use topical Ag sulfadiazine Disinfect whirlpools w/ iodine disinfectants, not recomm. b/c organism survives inside biofilm. Chlorination effective to kill pseudomonas P. Aeruginos sensitive to pH. Acetic acid (vinegar)!!!
#1 (most common) non-fermenting g(-), bacillus nosocomial infectious disease agent
Cell Features
Mycolplasma pneumoniae (EATONs agent & PPLO) Smallest, free-living organisms Pliable Cell membrane, contain sterol No cell wall G(null) Aerobic Motile Special nutrient req. cholesterol cell membrane
Colony Features
Growth leads to mulberry colonies w/ older colonies fried egg colony, slow growth
Lab Characteristic
Use gram staining to rule out any other causative agents Glucose fermentation(+) Tetrazolium dye reduction: turn blue to yellow Detected: Stain w/ fluorescent labeled ab, ELISA; latex agglutination

Humans are only reservoir Horizontal transmission via respiratory droplets mostly among teens & young adults.
Virulence Factors
1. Antimicrobial resistance: b/c of lack of cell wall, innately penicillin resistant. Does not make cell wall 2. Adhesion Protein P1: mediates adhesion to epithelial cells, ciliated cells & RBC 3. Production of H202 possibly contributes to mucosal damage & damage to RBC 4. Mycoplasma, survive intracellulary, cause most damage extracellularly
Associated Diseases
1. Atypical pneuomia (walking pneuomonia) most common cause, infection is mild or aymptomatic but can be fatal. Chest x-ray show unilateral lower lobar involvement Symptoms: interstitial pneumonia w/ nonproductive (persistant) cough & inspiratory crackles, fever, chills, headache & chest pain Complictions: lead to CNS & heart complications 2. Raynauds phenomenon occur to cold-agglutination antibodies, leads to necrosis of fingers & toes if in sickle cell anemia patients 3. Endocarditis (inflame. Of heart muscles) 4. Guillain-Barre Syndr. (asc paralysis more commonly associated w/ Campylobacter infection)

Ab & T cells important Associated w/ auto-ab production (IgM cold agglutinin) Cytokines activated EXCEPT IL-2
Doxycycline (leads to yellow teeth in children) Erythromycin for children & preg. women
G (-) bacilli
Helicobacter pylori
Cell Features
G(-) Pleomorphic (s-shaped, bacilli, curved rods, spirochete) Produce: corkscrew motility Microaerophilic (grow in 6% O2, 10% CO2) somewhat tolerant to stomach acidity
Colony Features
Organism grows on selective agar Chocolate agar or modified ThayerMartin incubate for a > 1 week under microaerophilic conditions (chocolatization detoxifies agar)
Lab Characteristic
Oxidase (+) Catalase (+) TSI (-) Urease (+) Nalidixic acid resist. Nitrate reduct. (-) Hippurate hydrolysis (-) Cephalothin sensit. Endoscopy: detect by biopsy. 14C-urea in food & look for 14CO2 in patients breath & serology

Human GI tract is reservoir. Oral fecal route is involved in horiztonal transmission (human to human)
Virulence Factors
1. LPS 2. Motility burrow through mucin layer stomach lining 3. Resistance to stomach acidity enhanced by movement of Helicobacter into & within the protective mucous layer of the stomach (not epithelia). Microaerophilic nature organism helps survival 4. Enzymes: a) Mucinase causes breakthrough of mucous layer in stomach (resist acid) b) Urease: stomach lining produce small amounts of urea .. leads to ulceration 5. Adhesion factors: attach to stomach (resist peristalsis) 6. Hemolysin (128kD) found w/ cytotoxin protein 7. Vacuolating toxin: 50% isolates virulence of strain (pathogenicity island* virulence, 8.Cag protein: stimulates host prod. of IL-8 & other signal transduction events 9. Catalase / superoxide dismutase: protects from intracellular killing phago. 10. Produce acid inhibitory protein (induce hypochlorhydrin)
Associated Diseases
1. Chronic Gastritis: Causative agent!!! Acute infection of stomach epithelium. Organism causes superficial mucosal inflammation & is non-invasive. Symptoms: nausea, abdominal discomfort. 2. Duodenal peptic ulcer: (#1 causative agent) follows chronic gastritis. Symptoms: burning abdominal pain 1-3hr after meals that may be relieved by eating & antacids. Complications include: bleeding, & perforation of GI tract 3. Gastric carcinoma: chronic gastritis

Immunocompetent patients have chronic inflammator y response w/ moncytes, macrophages & lymphocytes in stomach mucosa. Antibody formation not protective therefore patients after treatment may relapse
Combination of drugs: Pepto-bismol (Bismuth salts), amoxicillin, & metronidazole. Pen. Sensitive: Sub. Amox w/ Tetracycline Also include proton pump inhibitor ex. omeprazole
G (-) bacilli
Vibrio cholerae
Cell Features
g(-) comma shaped bacilli (curved rods) motile (flagella)
Colony Features
Grows blood agar Enrich in highly alkaline medium (loves higher pH) ThiosulfateCitrate-BileSucrose (TCBS) agar Can grow w/o salt HALOPHIC
Lab Characteristic
Oxidase (+) Lactose (+) Sucrose (+) Indole (+) Methyl Red (+) Urease (-) Chk rice-water stool for motile bacteria, culture on TCBS media & see if yellow b/c V. cholerae ferment sucrose

Human GI tract is reservoir for this organism Transmitted by oralfecal route (by drinking water & intaking raw & undercooked seafood, unpeeled fruits) Hortizontal transmission amongst humans Large inoculum (10^7 10^11 cells) b/c are killed by stomach acidity Exist in salt water for long periods of time / found associated w/ plankton, shellfish,
Virulence Factors
Cholera toxin (CT) A subunit (ADP-ribosylates) cytoplasmic G protein (G_s) regulates host adenylate cyclase. cAMP levels, induce intestinal cells to release Cl- ions into lumen. Toxin inhibits Na+ absorp, ions, water release (diarrhea!) LPS: endotoxin, 6 serotypes 01: NON-INVASIVE cause epidemics, no age preference but usually in children, preg. Women, long-term immunity. Non-01: sporadic infections 0139: INVASIVE infection in indiv. > 40 yrs, no immunity gained, possible reinfection. Flagelluem (H antigen): an adherence factor. Motility bacteria to enter into mucous layer, non-motile is avirulent. Adhesion factors: mediate bacterial adherence to SI epithelium. AF + CT to cause full-blown disease TCP-ACF: Toxin Co-regulate Pilis pathogenicity island.
Associated Diseases
Explosive Diarrhea! Cholera, remains in SI (duodenum) & non-invasive. rice water diarrhea (large vol. 1 liter/hr) rice: is mucus from intestinal wall. No fever involved Untreated patients may die in hrs due to hypotension, dehydration, & shock. Complications: - electrolyte imbalance - metabolic acidosis - hypoglycemia: kid - abortions Dehydrationleads to: - sunken eyes - loss of skin turgor - patient, comatose - death

Large inoculum needed to infect
Immediate & continuous IV or fluid replacement along w/ electroylates Replenish w/ NaCl / KCl add glucose to improve uptake of salts by intestinal cells. (try Gatorade!) Tetracycline is used for severe cases
Acidic polysacc. Capsule found ONLY in 0139 strain. It is INVASIVE. Can go out of intestine & cause infection Test question: Given tainted water w/ cholera w/ a dosage of 100 organisms, would a normal person be sick? No b/c it requires a lot more, but Shigella could kill you
Cell Features
Enterotoxigenic Escherichia Coli (E.Coli) AKA (ETEC) Dr. Trachmans favorite pet g(-) rod in pairs & chains anaerobic strains are motile
Colony Features
Grows on almost any medium, forms large gray colonies, on blood agar, some strains are hemolytic
Lab Characteristic
Oxidase (-) Lactose (+) Sucrose (+) ------------------------Indole (+) Methyl red (+) VogesProskauer (-) Citrate (-) {IMViC assays} ==> unique E.Coli ------------------------TSI butt & slant yellow w/ gas prod. H2S (-) Serology: Kaufman White Scheme REMEMBER: KOH K = capsule, fibriae O = LPS somatic H = H ag, flagella Culture on MacConkeylactose medium & blood agar

Most E.coli are harmless commensals of GI tract Some E.coli contain extrachromosomal DNA such as large ENT plasmids which enable E.coli to be pathogenic. Enterotoxigenic E.coli can colonize small intestines. Oral-fecal route by consuming contaminated water Hortizontal transmission from human to human TRAVELLERS DIARRHEA or AKA TURISTA
Virulence Factors
1. Heat-labile enterotoxin (LT): cholera-like binary toxin encoded in ENT plamids. It is cytotonic! Active A subunit ADP-ribosylates cytoplasmic G protein (G_s) regulates host adenylate cyclase. cAMP. (diarrhea!) 2. Heat-stable toxin (ST): encoded by ENT plasmids, activates guanylate cyclase & cGMP levels. Blocks ion uptake from lumen. Heat Looks like Rxn LT Cholera cAMP ST Yersinia E. cGMP -------------------------------------------LPS:endotoxin, Oag, serum resist Flagellum: H,ag bacteria enter mucus layer. w/ phase variation Pili: attachment to host cells. 2 Types Mannose Common pili Sensitive P pili Resistant Sex pili: conjugative plasmids transfer F+ plasmid or Hfr (donor, male) to F- (female) Fimbriae: attachment to host cells SI (tissue specific) CFA (colonization factor antigen) Antibiotic & heavy metal resist: Encode on conjugative plasmids Capsule: protect from acidicity E. coli produce hemolysins E. coli produce siderophores (Fe acquisition)
Associated Diseases
Enteritis or Travellers diarrhea (Turista). Noninvasive & remains in the lumen of SI. Symptoms: mild, watery diarrhea similar to V. Cholera EXCEPT the mucus.

sIgA against CFA & other bacterial components combats infection.
Fluid & electrolyte replacement : NaCl, KCL, glucose, & water. Antibiotics not given prophylaxively but use norfloxacin . Pepto-bismol (bismuth salts are inhibitory)
Cell Features
Enterohemorrhagic E. Coli AKA (EHEC) g(-) bacilli pairs or chains motile anaerobic
Colony Features
Grows on almost any agar forming large gray colonies
Lab Characteristic
Oxidase (-) Lactose (+) Indole (+) Methyl (+) Urease (-) TSI (-) for H2S Citrate (-) VogesProskauer (-) SORBITAL util (-) Serology 0157H7

Human GI tract is reservoir. Oral-fecal route by drinking contaminated water & undercooked Consume unpasteurized fruit juices, playing in contaminated water
Virulence Factors
Enterotoxins: lysogenic phage - Shiga-like toxin I (SLT-1): toxin f(x) in LI. Results: cleavage of euk 28s ribosomal RNA (60S). Mucosal cells poisoned, inhibits protein synthesis. Bloody stools. Enterotoxins enter bloodstream may be associated w/ kidney damage. - SLT-II (STX) : both of these are called VEROTOXIN b/c of their toxic effects on vero monkey kidney cells. - Enterohemolysin - LPS (endotoxin) - Pili: Adhesion, mediate bacterial (attachment to large intestinal epithelium. Plasmid encoded - capsule (possibly) - ACID RESISTANT, ~50 bacteria to cause disease (like Shigella). EHEC more acid resist - EAE genes (similar to EPEC) > attaching & effacing lesions
Associated Diseases
Hemorrhagic colitis: stays in lumen of LI & non-invasive. Blood diarrhea. Blood due to cytokine activity combined w/ SLT. Hemolytic-Uremic Syndrome: result in acute renal failure, hemolytic anemia & thrombocytopenia, 5% of cases. w/ platelet numbers. Complication (sequelae) seen in children & in immunocompromised or elderly.

Secretory IgA against bacterial components combats infection. Noninflammator y response to infection. Noninvasive
Fluid & electrolyte replacement. Antibiotics not used for prophylaxis. Prevention: - well cooked meals, burgers & pasteurized fruit juices Better treat: - fluids + salts - chlorinate water
Non-invasive - ETEC - Vibrio cholerae - EPEC
Invasive - EHEC - Shigella - Salmonella I M + + V + C +
Lactose Ferm. sugar Occurs Not occur Occurs slowly
Organisms E.Coli, Klebsiella, Enterobacter Shigella, Salmonella, Proteus, Pseudomonas (Acinetobacter) Serratia, Vibrio
E.Coli Enterobacter aerogenes
Cell Features
Salmonella Typhimurium AKA (S. enteritidis or S. enterica) g(-) rod in pairs or chains anaerobic motile
Colony Features
Grows on almost any agar medium large
Lab Characteristic
Oxidase (-) Lactose (-) Indole (-) Methyl red (+) VogesProskauer (-) Indole (-) Citrate (+) TSI (+) H2S Urease (-) Serology: Kaufman White Scheme REMEMBER: KOH K = capsule, fibriae O = LPS somatic H = H ag, flagella Culture stools on selective medium

Animal & human GI tracts are reservoirs (poultry, reptiles such as turtles & iguana). Oral-fecal route by consume contaminated water or food involved in hort. Transmission. Use antacids predispose for infection. Chronic carrier status Cutting boards/knives (need to clean w/ bleach) Raw eggs Survives freezing water, food or water for several weeks
Virulence Factors
LPS = exotoxin: mediates endotoxic shock, involves inflammatory response of intestinal mucosa. S. Resistant Invasion factor(s): bacteria invades hosts mucosal cells of the ileum & LI. Organism is able to survive in macrophages, not PMN. Flagellum (H ag): strong motility enable bacteria to enter into mucus layer. Inhibition of phagosomelysosome fusion: salmonella multiply in macrophage, then lyse macrophage & spread to nearby cells. Capsule (K ag): help bacteria survive stomach acidity Multi-drug resistant factors Enterotoxin: epidermal growth factor (EGFR) on host cell to bind to, leads to Ca in cell. leukotriene synthesis opens up Ca channels lead to rearrange actin. Results: leukotrienes inflammation. VIR genes turned on inside host cell ==> antigenic variation Pathogenicity island (SP-1, SP-2) Expression of genes can adapt to acidic environment
Associated Diseases
Non-typical Salmonellosis (Enterco-colitis): Initial invasion of mucosal cells of ileum & large intestines may be followed by systemic invasion. Symptoms: FEVER, nausea, water diarrhea, headache, enteric inflammation, & pus in stools. Entercocolitis may mimic appendicitis Bacteremia: intestines to blood stream. Leads to endocarditis, bile duct infection, septic arthritis, pneumonia. AIDS patient may have recurrent bacteremia Osteomyelitis: salmonella bone infections arising from bacteremia seen in sickle cell anemia patients Post-inf. Reiters Syndrom: arthritis, HLA-B27

Strong inflammatio n response w/ PMN & T-Cells. CMI is important b/c of intracellular location.
Most often is self-limiting Treatment enterocolitis: - fluid & electrolyte replacement Antibiotics dont eliminate Salmonella from GI but duration. Ciproflaxin, TMP-SMZ (bactrim) used for systemic infections Avoid raw eggs & use of antacids Wash hands before eating
Which organisms are associated w/ Reiters syndrome? Salmonella typhimurium & typhi
Cell Features
Salmonella Typhi AKA S. paratyhpi g(-) rod in pairs or chains anaerobic motile
Colony Features
Grows on almost any agar medium forms large gray colonies
Lab Characteristic
Oxidase (-) Lactose (-) Indole (-) Methyl red (+) VogesProskauer (-) Citrate (+) TSI (-) H2S Urease (-) Serology: Kaufman White Scheme REMEMBER: KOH K = capsule, fibriae O = LPS somatic H = H ag, flagella DNA probe for Vi antigen (capsule) WIDAL test: look for agglutinating ab acute & convalescent stages (refer to B. Pertusis) see 4x in ab titers, If (-) rxn then inconclusive.

Human GI tract is main reservoir for these organisms Oral-fecal route by consuming contaminated water & food. Hortizontal transmission Chronic carrier status in humans is possible survive in GI tract w/ predilection (bias) for gall bladder.
Virulence Factors
Vi antigen (capsule, hides surface markers, removed by boiling water). Bacteria resists LPS = endotoxin: major VF in mediating endotoxic shock, involves in inflammatory response of intestinal mucosa. May mediate serum resistance. Invasion factor(s): bacteria invades mucosal & epithelial cells of ileum & LI using this factor. Able to survive in macrophages but not PMN. Inhibition of phagosomelysosome fusion: Salmonella multiply in macrophage, then lyse macrophage & spread to nearby cells Flagellum (H ag): bacteria enters mucus layer. Has phase var. similar to E.Coli Multi-drug resistant factors: plasmid encoded beta lactamase & chloramphenicol transferase. Ability to adapt to acidic environment expressed by genes
Associated Diseases
Typhoid Salmonellosis (Enteric fever) & paratyphoid fever. 2 stages: Invades Peyers patch of ileum & LI infects various organs & tissues: liver, kidneys, spleen, bone marrows, gall bladder, skin (ROSE SPOT TRUNK) & heart Wk 1-3 2-3 2-3 2-3 4 Issue Incubation Hepatoslenomegaly Bradycardia ROSE SPOT on trunk Secondary infections GI tract
Host Def.Im.
Stomach acid kills Salmonella. Large amounts of inoculum causes the infection
Treatment / Prevent
Antibiotics ciproflaxin Systemic Inf: - TMP-SMZ (Bactrim) - Amoxicillin - chlororamphenicol Misc notes: Ciproflaxin eliminates carrier state
Symptoms: - FEVER - abdominal pain - headache - water diarrhea - enteric inflammation - pus in stool Bacteremia: intest. to blood stream, subacute endocarditis, bile duct inf. Reiters Syndrome: arthritis (see S. enterica) Abortion: enteric fever
* Most invasive! Enterics are resistant to bile
Cell Features
Shigella species g(-) rods in pairs or chains non-motile Lactose (-) NONMOTILE anaerobe
Colony Features
Grows on almost any agar forming large gray colonies. On EMB, organism is colorless or white
Lab Characteristic
Oxidase (-) Lactose (-) Indole (-) Methyl red (+) Urease (-) TSI (-) for H2S Citrate (-) VogesProskauer (-) NON-MOTILE!!! SERENY TEST: (inoculate guinea pig or rabbit eyes) Get specimen from rectal swab, sigmoidoscopy

Human GI tract & GI tracts of higher primates Can survive for months, but it is delicate. Five Fs: - food - fingers - feces - flies - fomites Common among homosexual men
Virulence Factors
Enterotoxin: Shiga toxin has same activity. RNase activity cleaves euks 28S ribosomal RNA. Stops protein synthesis, results in bloody diarrhea. Verotoxin: ONLY S. dysenteriae (see chart below) LPS (endotoxin): epithelial necrosis end of ileum & colon. Polysach. somatic O antigen to avoid phagocytosis, serum resistant Invasion factors: similar to EIEC. Plasmid encoded & mediates invasion & destruction of epithelium of colon. Commandeering of Actin filaments in host cell for mobility in host cell ==> helps spread to nearby cells Shigella are able to survive acidity of stomach: infection requires very small inoculum 50-300 cells Multi-drug resistance plasmids
Associated Diseases
1. Bacillary Dysentery (shigellosis): invades mucosa of LI but not underlying muscle Symptoms include: Watery diarrhea progresses to bloody diarrhea, fever, & inflammation w/ pus in stools. Toxin kill mucosal cells of intestine. Often found in children & elderly. 2. Hemolytic-Uremic Syndrome: Shigella infection may result in actue renal failure, hemolytic anemia, & thrombocytopenia. 3. Post-Shigellosis Reiters Syndrome: arthritis associated w/ HLA B27

Strong acute inflammatory response to infection by PMN. Secretory IgA against bacterial infection CMI important b/c of intracellular location
Treatment Prevent
Infection is self-limited. Fluid & electrolyte replacement. Antibiotics shortens duration but not lessen intensity Bactrim (TMP-SMZ) used for serious cases, stop transmission . Nalidixic acid or newer quinolones Prevent from consuming uncontaimin ted food & water
-------------------Innately non-motile but once inside the host becomes motile b/c of actin filaments
Shigella Type S. boydii S. flexneri S. sonnei S. dyenteriae
Serogroup C B D A
# serotypes 18 14 1 12
Comments Most common in developing countries Most common serogroup in US, acquired when traveling to endemic area (NON-MOTILE!!!) Most common in remainder of world, most pathogenic, most invasive, produces Shiga toxin (LACTOSE (+)!!!)
Test question: Which pair organisms are associated wit h hemolytic-uremic disease? Shigella dysenteriae & EHEC
Cell Features
Bacteroides fragilis g(-) slender rods, pleomorphic obligate anaerobe non-motile capsule NO endotoxin activity b/c it lacks Lipid A !!!
Colony Features
Grows anaerobically on complex agar medium, brain heart infusion forms gray glistening colonies due to capsular polysacch.
Lab Characteristic
Anaerobic growth, penicillin resistant Superoxide dismutase (+) Catalase (+) Indole (+/-) Growth in 20% bile Antibiotic Resistant - colistin - kanamycin - vancoymcin

Human GI tract is resvoir for Bacteroides MOST numerous bacterial species in human body Outnumbers E. coli in colon. Alcoholics, immunocompromised patients, patient w/ anesthesia can lead to pulmonary infections (opportuntistic) Mixed w/ an/aerobes May have synergistic interaction
Virulence Factors
1. Polysaccharide capsule (K antigen): major VF w/ anti-phagocytic activities. Attach to peritoneal mesothelium 2. catalase & superoxide dismutase: allows organism to remain viable for days w/ O2 (aerotolerant) 3. Enzymes contribe to Bacteroides (act as spreading factor): - heparinase for intravascular clotting - collagenase - hyaluronidase - lipases - nucleases (DNases, RNases) - Pili / fimbriae
Associated Diseases
1. Intraabdominal Disease (abscesses): opportunistic, associated w/ post-op. peritonitis, inf. abdomen w/ intestinal contents gunshots, stab wounds, surgery, cancer, (80% by b. fragilis) UTI in women lead to pelvic abscesss (PID), & brain & lung infection 2. Soft tissue & cellulites: mixed infections w/ peptostreptococcus, bacteroides, fusobacterium, & actinomyces (all anaerobes) Post-opt., cutaneous & or mucotaneous infections. UTI 3. Bacteremia: may cause endocarditis & brain abscesses 4. Upper/Lower infection 5. Crepitant cellulites (especially in foot), usually post-op inf. 6. DIABETIC FOOT INFECTIONS (FECAL FALL OUT)!!!

Both humoral & CMI involved in combating Bacteroides infections
Debridgement & surgical drainage before antibiotic treatment - clindamycin Seriously ill: - chloramphenicol Alternatives: - erythromycin or moxalactam
-------------------Obligate anaerobe :: facultaitive & anaeroebe (10,000: 1 ratio)
Cell Features
Proteus mirabilis g(-) pairs or chains rods facultative anaerobe highlymotile b/c peritrichou s flagella
Colony Features
Grows on blood agar forms large swarming colonies w/ blood agar only w/ putrid odor
Lab Characteristic
Oxidase (-) Lactose (-) Indole (-) Methyl red (+) Urease (+) TSI & SIM (+) for H2S Citrate (+) VogesProskauer (-) Phenylalanine deaminase (+) distinguish from P. vulgaris!!!

Normal flora human LI (colon), crap found in soil & water. Nosocomial or iatrogenic infection UTI can happen in healthy & immunocompromised w/ large inoculum ==> opportunistic Hortizontal transmission
Virulence Factors
1. Urease: splits urea to NH4 ions ==> alkaline urine promotes urolithiasis (kidney stones). Destroys the urinary epithelium & cause infection & impair kidney fxn 2. Strong motility: movies up urinary tract 3. LPS (endotoxin)
Associated Diseases
1. Urinary tract infections: a) pyelonephritis b)cystitis. Infections may be acute or chronic. Symptoms: pain fever pyuria hematuria urination (synchuria) 2. Urolithiasis: MgNH4 phosphate salts form kidney stone due to NH4 3. associated w/ bacteremia, pneumonia, endocarditis

IgA, IgG, made against various bacterial components. PMN involved in acute infections (pus is formed) Macrophage s & T cells respond to chronic infections
Ampicillin for cystitis Bactrim (TMPSMZ) for pyelonephritis
UTI: contamination with fecal matter a) lower UTI = cystitis, infection of urinary cyst, bladder b) upper UTI = pyelonephritis, serior infection see blood, pus in urine c) renal or kidney stones = urolithiasis (struvite) & apatite, formation due to production of urease (ie Proteus)
Cell Features
Proteus vulgaris g(-) rod, pairs, chains facultative anaerobe motile b/c peritrichous flagella
Colony Features
Grows on blood agar forms large swarming colonies w/ blood agar only w/ putrid odor
Lab Characteristic
Oxidase (-) Lactose (-) Indole (+) Methyl red (+) Urease (+) TSI & SIM (+) for H2S Citrate (-) VogesProskauer (-) Phenylalanine deaminase (-) distinguish from P. mirabilis!!!

Normal flora of human LI (colon) Nosocomial or iatrogenic infection UTI occur in immunocompromised Hortizontal transmission
Virulence Factors
1. Urease: splits urea to NH4 ions ==> alkaline urine promotes urolithiasis (kidney stones). Destroys the urinary epithelium & cause infection & impair kidney fxn 2. Strong motility: movies up urinary tract 3. LPS (endotoxin) 4. Multiple drug resistance
Associated Diseases
1. Urinary tract infections: a) pyelonephritis b)cystitis. Infections may be acute or chronic. Symptoms: pain fever pyuria hematuria urination (synchuria) 2. Urolithiasis: MgNH4 phosphate salts form kidney stone due to NH4

Ampicillin for cystitis Bactrim (TMPSMZ) for pyelonephritis
Proteus mirabilis Indole (-) Citrate (+) Phenylalanine deaminase (+) distinguish from P. vulgaris!!!
Proteus Vulgaris Indole (+) Citrate (-) Phenylalanine deaminase (-)
Cell Features
Europathogenic E. Coli (UPEC) Extraintestinal E. coli infection g(-) rod, pairs, chains facultative anaerobe motile
Colony Features
Grows on almost any agar surface forming large gray colonies. On EMB, have metallic sheen (b/c eosin) Enterobacter yields larger colonies
Lab Characteristic
Oxidase (-) Lactose (+) Sucrose (+) Indole (+) Methyl red (+) Urease (-) TSI (-) for H2S Citrate (-) VogesProskauer (+) This unique!!!

Normal flora of human LI (colon) Nosocomial or iatrogenic infection UTI occur in immunocompromised primarily Hortizontal & Vertical transmission
Virulence Factors
1. Polysaccharide capsule (more infectious): strains w/ K1 capsule contains K1 sialic acid associated w/ bacterial meningitis. E. coli w/ K1 are NOT immunogenic, protects against phagocytosis & against complement-mediated lysis. 2. Hemolysins: release cytokins, leads to inflammation Alpha hemo: disrupts lymphocytes Beta hemo: membrane-bound & h& inhibits PMNs 3. Motility: flagella (H antigen) b/c of phase variation 4. LPS (endotoxi) most inf. isolates 04.05.075 5. Pili a) P (PAP) pili involved in UTI, attaches to uroepithelia. These strains can cause pyelonephritis P Pili are mannose resistant Type 1 pili used for adhension (see bolow) 6. S. Fimbria: not well reconigzed 7. Siderophores: chelate host Fe released by RBC (hemolysins), & take from transferrin & allow Fe uptake by E. Coli 8. Serum resitant: resist oposonization / destruction by host complement factors or due to k1 capsules
Associated Diseases
1. Urinary tract infections: (#1 cause of UTI, 80-90%) a)pyelonephritis infection of kidneys. Infections may be acute or chronic. Most nosocomially acquired infections are complicated & present as pelonephritist. They are opporunitic & infect 2. Urolithiasis: MgNH4 phosphate salts form kidney stone due to NH4 immunocompromised b) Bacteremia & sepsis: (#1 causative nosocomial agent) UPEC bacteremia is complicated. c) Neonatal meningitis (#2 causative nosocomial agent) cause sepsis & death. Need lumbar puncture: CSF PMN, glucose d) Opportunistic pheumonia similar ot Klebsiella pneumoniae

Ampicillin for cystitis Bactrim (TMPSMZ) for pyelonephritis Ampicillin & gentamycin -
L theZoonotic (GI infect) Campylobacter jejuni
Cell Features
g(-) PLEOMORPHIC Curved rods, spiral forms w/ coccobacilli Microaerophilic (6% O2 & 10% CO2) Motile (can penetrate SI & multiply) Darting motility
Colony Features
CAMPY agar supplement w/ blood & other nutrients Grows from 4 - 42C to inhibit other bacteria

Oxidase (+) Catalase (+) Hippurate Hydrolysis (+) Urease (-), [differentiate from helicobacter] Fecal specimen: CAMPY AGAR +vancomycin +cefoperazone Grows @ 42C, O2 & CO2 Animal GI tract (zoonotic infection) Contact w/ infected: animals, dogs, cats, fowl (chicken), but NOT eggs! Even animal scratches (did you see her nails?) Improper handling: - utensils & cooking Raw unpasterurized milk or water contaminated (feces) b/c bacteria survives in milk for up to 5 weeks when stored at 4C Sensitive to chemical disinfectants, acidity, & chlorination Relate to spontaneous abortion(effect) infant b/c infected genitourinary tract xover placenta Oral-fecal route (man to man transmission) * in children
Virulence Factors
1. CT like enterotoxin 2. cytotoxin (not Shigalike) results in bloody diarrhea 3. LPS (endotoxin) 4. Flagellum: bacterial motility; darting movement 5. adherence factor 6. grows well w/ bile 7. can be invasive
Associated Diseases
1. ENTERCOLITIS: acute infection of epithelium of SI (jejunum & ileum) & LI. Common in children 2. Enterotoxin invades the epithelial cell, superificially Symptoms: - fever - nausea - abdominal discomfort - watery diarrhea Severe cases: - cytotoxin production (bloody diarrhea + pus) or enteric inflammation & last for about a week (self limit) - Extraintestinal disease: survives intracellularly 7days 2. Guillain-Barre Syndrome: - ascending paralytic disease - viral inf. (influenza, EpsteinBarr Virus EBV) 3. Abortion: organisms invasiveness can invade fetus or across placenta during a septicemia or ascending inf. 4. Reiter syndrome: - post-infection, arthritis, associated w/ HLA-B27

Acute inflammatory response by PMN. Both Tcell mediated immunity & secretory IgA & IgG.
Infection is selflimiting but requires fluid & electrolyte replacement. Erythromycin
Zoonotic (GI infect) Yersinia Enterocolitica
Cell Features
g(-) short rod facultative anaerobe motile non-motile at 37C or in host
Colony Features
Grows on blood agar No siderophore, so needs iron for growth Tolerates at cold storage 4C

Oxidase (-) Catalase (+) Lactose (-) Urease (+) Methyl red (+) VogeProskauer (-) Animal GI tract is reservoir therefore zoonotic infection Water contaminated w/ animal feces may also be involved. Oral-fecal route involved man-man transmission Raw milk (also from cold-stored blood) Y. enterocolitica is NOT need insect vector for transmission
Virulence Factors
1. V and W antigens: unknown f(x) but essential (found in Y. pestis) 2. Enterotoxin: YST is heat-stable enterotoxin similar to ETEC (E.coli) 3. LPS (endotoxin) 4. Flagellum: mediates motility outside of host, but non-motile at 37C 5. Serum resistance: (plasmid encoded) 6. YadA gene: outer membrane protein, adhesion to epithelial cells 7. Genes, invasiveness: - Inv gene (invasion), surface protein - Ail gene (adherence invasion locus), facilitate entry into specific cells 8. FACULTATIVE INTRACELLULAR 9. Pathogenicity island 10. Type III secrete proteins VF regulated by calcium & by temperature
Associated Diseases
1. (Hemorrhagic) Enterocolitis: Acute infection of the epithelium of the SI (ileum) & LI. Symptoms of GI tract include: fever, nausea, abdominal discomfort, headache, water diarrhea which may be bloody + pus (enteric inflammation). Y. enterocolitica is destroyed by stomach acidity, large inocula 10^9 cells to be infected. 2. Terminal ileitis: lead to peritonitis 3. Septicemia: rare; lesions internal organs 4. Reiter syndrome: - post-infection, arthritis, associated w/ HLA-B27 Bacteremia w/ this organism ; therefore, can be blood-borne by transfusions

Acute inflammatory response by PMN. Both Tcell mediated immunity & secretory IgA & IgG.
Infection is selflimiting but requires fluid & electrolyte replacement. W/ Y. enterocolitica sepsis, gentamycin of Bactrim used Use good hygiene
Fever related infection Brucella Species
Cell Features
g(-) coccobacilli aerobic non-motile
Colony Features
Grows slowly on blood agar Requires blood media

Oxidase (-/+) Cabalase (+) Urease (+/-) TSI (+/-) No fermentation N03 reduction LPS: associated antigens, A = abortus antigen & M = (melitensis) antigen, are present Animals are reservoir for Brucella species. Zoonotic infection of man occurs by contact w/ infected farm animals such as cows, goats, & pigs. Hygiene (handwash!) Ingestion of raw milk Erythritol levels in placenta (breast, uterus, epididymis)
Virulence Factors
1. Superoxide dismutase: Allows survival w/in PMN & phagocytes 2. Survives in reticular endothelial cells. B. Abortus block acidification. Intracelluarly releases 5 & inhibits myeloperoxidase halide system to generate toxic oxygen. 3. LPS (endotoxin) 4. Serum resistance
Associated Diseases
1. Brucellosis: Enteric Fever simlar to Typhoid Fever. Systemic infection involves multiple organs, include GI tract, liver, (RES = reticular epithelial organs. Organs , macrophages (spleen, liver, bone marrow, lymph nodes, kidneys) May result in enlargement, endocarditis & p.neumonia. Symptoms: - malaise, chills, sweats, & fatigue, weight loss, nonproductive cough & fever (intermittent). 2. UNDULANT FEVER/ BANGS DISEASE / MALTA FEVER - fever is intermittent or diurnal. Untreated, results in chronic flue conditions. May also see bone & joint infections, severe depression, & osteomyelitis. Granuloma formation in liver, spleen, bone marrow & changes in the organs.

Ab (IgM, IgG) CD4 & CD8 Tcells, cytokines IFN gamma, & IL-2. Granulomas are formed by delayed hypersensitivity rxn. IgG indicates relapse
Treated w/ (a) oral doxycycline + intramuscular gentamycin or (b) doxycycline + rifampin difficult to treat takes 4-6 weeks & it is intracellular Pregnant women should use: Bactrimn + gentamycin Best to pasteurization of milk & vaccination of farm animals
Brucella infections leads to CHRONIC disease (test bank: 10 day periodicity) Infect a variety of animals & can cause disease in humans as opportunistic infections. Under goes UNDULANT FEVER (waves peaks & valleys) B. abortus (Bang & Malta fever) - Primarily cause disease in cattle - abortion in animals, rich in euorthrodol - mild disease w/ suppurative complications uncommon, self-limited B. melitensis - more infectious but primarily in goat & sheep - severe acute disease w/ complications such as granuloma formation, becomes chronic B. suis - infections in swine - suppurative, destructive disease w/ granuloma formation B. canis - dogs, foxes, coyotes - mild disease. Suppurative complications
Human Disease
Rickettsiallike agent Coxiella Burnettii
Cell Features
g(-) coccobacilli aerobic related to Rickettsia
2 phases growth
Colony Features
Grows in cell culture or in animals or in embryonated eggs / tissue culture (needs to grow w/ cells no artificial media acceptable, not even w/ blood)
Lab Characterist
Weil-Felix Reaction (Rickettsia have antigen on surface that cross react w/ antigen on certain Proteus species) Ox-19 (-) Ox-2 (-) Ox-K (-) Indirect fluorescent antibody kit on smear, detection important (grown in yolk sacs, look for complement fixing ab, inject sputum, blood into hamster)

Animals are reseservoir for Coxiella. Zoonotic infection. Infected farm animals cows, goats, pigs, rabbits, birds. Transmission occurs by aeorsoles (contain spores) from dried urine, feces or milk. Ingestion of raw milk from infected animal Spores / cysts survives at 60C for 1 hr therefore pasteurization at 62.9C Test Q Characteristic: - Not vector borne, difference btw Rickettsial disease, ticks can be involved in transmitting Coxiella. Ticks are NOT direct source. Tick feces on cattle hides get transmitted when human inhales these spores.
Virulence Factors
1. Superoxide dismutase - survival within the acidic phagolysosome 2. * ACIDOPHILIC - spore taken up by phagocyte, metabolically activated by acid of phagolysosome (multiplies) 3. LPS (endotoxin): phase variation a) phase I: highly inf., surface antigen blocked b) phase II: less inf. 4. Cysts or spores allow for Coxiella to survive for long periods of time under adverse conditions
Associated Diseases
1. Q (Query) Fever: acute febrile disease: symptoms include: flu-like disease w/ fever, headache, chest pain, chills, malaise, severe sweats. VERY INFECTIOUS! 10 bacteria may cause illness. Usually self limiting, but may become latent infection & chronic, which may reactived (use cortisone). 2. Q Fever Pneumonia: Atypical pneumonia w/ non-productive cough, inspiratory crackles & flulike symptoms. No fluid in lungs 3. Q Fever hepatitis/ Hepatosplenomegaly: Fever & observe liver granulomas (upon biopsy), very rare as result of chronic latent infection 4. Q Fever endocarditis (subacute): culture (-), associated w/ chronic (latent) infection, valvular heart disease w/ preexisting damage of valves. Incubation months to years. 5. Chronic (latent) infection: osteomyelitis, neurological symptoms, heptatis

Igm & IgG useful. CMI and cytokines lead to intracellular killing of Coxiella. Granulomas formed by DTH Rxn
Tetracycline for pneumonia Doxycycline + TMP-SMZ (Bactrim) w/ min. 2 years Delayed Type Hypersensitivity
1. spore/cyst - Dry phase - animal urine 2. veget. phase Not effective spore compare w/ other endospores b/c this is g(-) ** Obligate Intracellular! (can also exist outside of cell, doesnt need to be spread by any vector)
Cell Features
Francisella Tularensis g(-) coccobacilli (pleomorphic, very small) facultative anaerobic, but prefers O2 non-motile
Colony Features
Grows on medium containing blood, glucose, & cysteine (recommend chocolate agar + cysteine)
Lab Charact.
It is hazardous!

Transmitted by direct method or by vector. Wild animals are reservoir. Zoonotic infection of man occurs by contact w/ infected wild animals Duch as beaver, rabbit, squirrel & deer. RABBIT FEVER can be fatal! Transmissin occurs by tick, mosquito, or fly vectors. Contaminated water (ex. Contaminated H20) maybe envolved in transmission also in stagnant water. Transmitted via aerosols Inoculum size to be ill: 10 bugs tick bites 50 bugs if inhale 10^8 ingested
Virulence Factors
1. Lipid capsule: blocks phagocytosis & blocks opsonizaiton 2. LPS (endotoxin) 3. Survive in monocytes and PMN (protect from ab & complement). Resistant to lysosomal oxidans, include HCl by PMN and inhibits phagosome-lysome fusion
Associated Diseases
1. TULAREMIA (RABBIT FEVER): 2. Ulceroglandular tularemia: contact w/ infected animal, arthropod bite, open ulcer at entry site (ex. Lower extremity or trunk), possible bacteremia 3. Oculoglandular tularemia (eye): conjuctival ulcer, regional lymph nodes, opens & drains bloodstream, liver, spleen, lungs. Invasiness & goes to the blood stream. 4. Pneumonic tularemia: if reach lungs by blood or by respiratory route (aerosol) then spread by person by person. High mortality rate. Especially inhaled version! 5. Typhoidal tularemia: ingest food or water (larger inoculum size) GI & fever symptoms can cause sepsis w/ multi-organ involvement, even pneumonia 6. Glandar: painful adenopathy w/ overlapping ulcers

IgM & IgG are ineffective against infection. Granulomas are formed by DTH rxn. T cell mediated immunity is important to activate phagocytosis for intracellular killing,
Difficult b/c intracellular Antibotics: tetracycline gentamycin streptomycin chloramphenicol penicillin (some) Prevention: Handling animals, avoid infected animals Vaccine: Live-attenuated vaccine used only on people at risk animal handlers
Cell Features
Bartonella henselae g(-) curved rods aerobic motile twichting motility
Colony Features
White, rough, mixed w/ tan circular Grow slowly on selected blood agar 15% CO2 Facultative intracellular pathogen
Lab Charact.
Oxidase (-) Catalase (-) Easy to see w/ Ag impregnation techniques

Cats (blood) are reservoir Zoonotic infection of man occurs by the bite or scratching of an infected cat Man to man transmission NOT observered Can survive in saliva, inhale lice feces, crushed lice Causes conjuctiva infection
Virulence Factors
1. LPS (endotoxin) 2. Type IV pili adhesion, twitch motility 3. Facultative intracellular pathogen
Associated Diseases
1. Bartonellosis (CAT SCRATCH FEVER): symptoms begin 2 weeks exposed. Local lymphadenopathy (lymph nodes), fever, & pustules at scratch site. It is self-limiting last months to years. Forms granuloma. 2. Bacillary angiomatosis: in immunocompromised patients (AIDS) observe chronic spreading cutaneous & visceral lesions, Kaposis sarcoma-like lesions may appear, differ histologically. Bacteremia & sepsis may also occur in these patients 3. Sub-acute bacterial endocarditis 4. Bacillary peliosis hepatits (Peliosis): cyst of blood-filled granulomas 5. Conjunctiva infection (Oculoglandular syndrome): swelling of eye, jaw, cervical lymph nodes
Self-limiting Can scratch disease treat w/ needle aspiration but NO antibiotics Bacillary angiomatosis & sepsis treated w/ erythromycin
Cell Features
Pasteurella multocida g(-) coccobacilli w/ bipolar staining facultative anaerobe non-motile intracellular pathogen
Colony Features
Grows on blood agar produce yellow colonies w/ musty odor Grows best w/ 02 at 37C
Lab Charact.
Oxidase (+) Catalase (+) Indole (+) Methyl red (-) Nonhemolytic Sucrose utilization (+)

Animals & birds are reservoir, upper respiratory tract & saliva are involved in transmission. Zoonotic infection of man occurs by the bite or scratching by infected dog or cat. Man to man transmission not observed Commensals in some animals
Virulence Factors
1. LPS (endotoxin) 2. Large polysaccharide, capsule: antiphagocytic 3. Pili mediates attachment 4. beta lactamase: in some strains
Associated Diseases
Acute cellulitis: symptoms include erythrema, swelling, & pain at bite / scratch site. Usually the host injuries occur on leg, arm, or face. Associated w/ severe bites! Complications include: - tendonitis - osteomyelitis - abscess formation Leads to systemic septicemia or meningitis AIDS patient: complication includes sepsis

T-cell mediated immunity is important. Strong acute inflammatory response w/ PMN is very important
Penicillin or ampicillin & tetracycline. Allergic patients - doxcycline Avoid contact w/ wild & domestic animals & birds
Flea borne
Yersinia pestis
Cell Features
g(-) short coccobacilli w/ bipolar staining facultative anaerobe non-motile facultative intracellular pathogen
Colony Features
Grows on blood agar. Epicellulargrows both on tissue & on plates Grows best at 28C w/ oxygen
Lab Charact.
Oxidase (-) Catalase (+) Lactose (-) Urease (-) Methyl red (+) VP (-) Gram satn & Waysons satn to look for bipolar cells Direct immunofluorescence

Animals are the reservoir Zoonotic (also Vector-borne infection) Fleas from infected animals RODENTS, rats, & squirrels involved in transmission of disease to humans. Fatal transmission, & survives for several months in infected carcasses, sputum, & flea feces. May cause enteric disease from ingest contaminatation. Inhalation of aerosolized Y. Petsis from infected humans or while handling infected live animals carcasses. Pneumonic Plaque (rare & deadly!) Sylvatic plaque (transmit by fleas on rabbits, squirrels vs. urban plaque spread by rats) Flea jumps onto human. Then spread human to human. Organism survives in animal blood & flea gut
Virulence Factors
1. LPS: fatal, septic shock 2. V and W antigens: exact f(x) unknown but involved in extracellular survival as well as intracellular survival & multiplication in macrophage; Resists phagocytic killing & are facultative intracellular pathogens. 3. Coagulase: blood to clot during flea bloodmeal, regurgitate into the next bite 4. Fibronolysin: produced, breaks the clot & spreads 5. Iron acquisition: - takes up iron (hemin) by siderophore-independent Produce siderophore (only one) 6. Protein capsule-complex: Fraction1: not produced in rat flea plasmid encoded allows for survival inside of phagocytes 7. Promote invasion & proliferation within host cells and resistant to killing by host LCR plasmid products are expressed at 37C and at Ca++ which directs V and W antigen synthesis. 8. Pesticin: bacteriocin, makes the organism more virulent 9. pur protein: allows uptake of adenine & guanine nucleotides 10. pigment production 11. Pathogencity island 12. YopE, disrupt actin filament 13. YopJ/P: initiate apoptosis 14. Plasminogen activator 15. Type III: secretion system
Associated Diseases
BUBONIC PLAGUE: w/in 2-3 days of flea-bite. Symptoms include: fever, chills, painful lymphadenitis (buboes). Inguinal, axillary, femoral & cervical lymph nodes involved, & may swell. Bacteremia, sepsis follows. Vasculitis may lead to gangrene (Black death, necrosis of capillaries, blacken body). Infection is fatal. If swallowed, stools maybe bloody + pus (enteric inflammation). May last for weeks w/ treatment. Septic plague: NO occurrence of buboes, found in children bites from flea. Leads to intravascular coagulation w/ vascular & renal collapse. Pneumonic plague: already in lungs, inhales. Results in bronchopneumonia. Symptoms include: fever, cough w/ blood & loaded w/ bacteria. Deadly & rarest form. HIGHLY INFECTIOUS! 90-100% death rate. Sylvatic plague: fleas on rabbits, wild rats to fleas on urban rats to human fleas to human.

Granulomas are result of DTH. Acute inflammatory response by PMNS. Both CMI and sIgA and IgG are important against infection.
ASAP! w/ Streptomycin Chloramphenicol Tetracylcine Hypotension use dopamine. Disease is prevented by rodent control but also need to control rat flea & human flea. Use pesticides.
Cell Features
Rickettsia Typhi Aka R. Mooseri Vec./spec Flea-ty end ENDEMIC Radiates outward g(-) small coccobacilli non-motile aerobic OBLIGATE INTRACELLULAR PATHOGEN
Colony Features
Grown in cell culture
Lab Charact.
Weil-Felix Rxn (agglutinate w/ Proteus vulgaris) ex: Ox-19 (+) Ox-2 (-) Ox-K (-)

Vertebrate animals are reservori for R. typhi in particular rats. Zoonotic infection of man occurs by bite of infected flea (vector). In infected flea (rat, cat). Maybe transmitted by transovarian method (moma fly to baby fly) Also flea bites (w/ feces) transmitted into bite wound.
Virulence Factors
1. LPS (endotoxin) 2. Factors inducing phagocytosis. Inside phagocytes the organism survives & enters into the host endothelial cells. Evade host cell lysis (escape from cell). 3. Produe phospholipase A (lecithinase) which lyses phagosomes enabling rickettsia to enter into host cell cytoplasm. 4. Organism able to survive in rat blood & flea feces 5. Loosely adherent slime layer.
Associated Diseases
Highly infectious (but lowest pathogenicity of the Rickettsia). 10 organisms to cause disease! 1. Endemic flea-borne TYPHUS aka Murine typhus Systemic inf. following a flea bite. Rickettsemia causes vasculitis of the capillary beds of many organs particularly of the liver & skin. Typhus produces fever, chills, headache, & macular rash mosly on trunk (hallmark) and may eventually spread outward to extremities. This differs from Spotted Fever, rash start on palms & soles & radiate inward to trunk.

Ab may be important initial barriers against infection. Previous infection confers longlasting immunity. Observed crossimmunity w/ R. prowaseckii.
Oral doxycycline (makes teeth yellow in children) Preg. Women are treated w/ chloramphenicol Killing rat is not enough, b/c flea could jump to humans.
Louse-Borne Bartonella Quintana (Rochalimaea Quintana) Trench warfare Epidemic responsible
Cell Features
g(-) curved rods motile (twitching) aerobic OBLIGATE INTRACELLULAR PATHOGEN
Colony Features
Grows very slowly on selective agar medium
Lab Charact.
Oxidase (-) Catalase (-)

Humans were thought to be only reservoir BUT cats too. Indirect transmission from man to man occurs by BITE of the VECTOR, the body louse
Virulence Factors
1. LPS (endotoxin) 2. Facultative intracellular pathogen
Associated Diseases
1. Bartonellosis Trench Fever (5 day fever). Remember it is facultative intracellular & has periodicity cycle in 5 day periods. Symptoms include fever, headache, exhaustion. temp. during this periodicity (Quintana), chills severe bone pain & transient rash on trunk & may see splenomegaly & myalgia. Self limiting but may relapse. 2. Reemerged in AIDS patient & homeless (immuno-compromised)

Both IgM and IgG are important
Doxycycline or chloramphenicol Pregnant women - erythromycin
Inhalation of louse feces is another method of transmission. Epidemics is common. Associated w/ filth & poor santition.
Louse-Borne Rickettsia prowaseckii Mnemonic Vect/Spec/dis Lousy pr-epi Epidemic responsible Spreads outward
Cell Features
g(-) very small coccobacilli non-motile aerobic OBLIGATE INTRACELLULAR PATHOGEN
Colony Features
Lab Charact.
Weil-Felix Rxn (agglutinate w/ Proteus vulgaris) ex: Ox-19 (+) Ox-2 (-) Ox-K (-)

Humans are primary animal reservoir but other animals can also be reservoir. Flying squirrels. Zoonotic infection of man occurs by bite of infected louse (vector). Arthropod likely to be squirrel flea.
Virulence Factors
1. LPS (endotoxin) 2. Produce factors inducing phagocytosis. Inside phagocytes the organism survives and enters into the host endothelial cells. Evade host cell lysis. 3. Produces phospholipase A (lecithinase) which lyses phagosomes enabling rickettsia to enter into host cell cytoplasm. 4. Organism is able to survive in rat blood & flea feces 5. Slime layer More life threatening: Bartonella Quintana
Associated Diseases
1. Epidemic louse-borne typhus:Systemic f(x) following a louse bite. Rickettsia cause vasculitis of capillary beds of many organs particularly of the liver & the skin. Clotting abnormalities Symptoms include: - high fever, chills, heaches, & pain Rash mostly on trunk (key feature!) & spreads outward toward extremities EXCEPT face, soles & palms. (differs from Spotted Fever which starts from palms & soles & radiate inwards to trunk) See neurological changes include delirium & stupor. During cold weather may lead to gangrene of feet & fingers. 2. Brill-Zinsser Disease: Reactivated epidemic typhus (BuZy Pissing) (less severe than primary infection) May occur years after initial disease. Chronic carrier w/ less intense rashes b/c of partial immunity. 3. Copmlications: CNS dysf(x), myocarditis

Ab may be important initial barriers against infection Previous infection confers longlasting immunity
Oral doxycycline Pregnant women are treated w/ chloramphenicol
Infected louse may be transmitted to man via inhalation of dried lice feces or by bite wound or crushed into the skin. NOT passed transovarian Unlike other rickettsia diseases: can also see man to vector to man transmission. Still needs the vector as source!
Tick-Borne Rickettsia rickettsii
Cell Features
g(-) very small coccobacilli
Colony Features
Lab Charact.
Weil-Felix Rxn (agglutinate w/ Proteus vulgaris) ex: Ox-19 (+) Ox-2 (+) Ox-K (-)

Animals (wild mammals & birds) & hard ticks Zoonotic infection of man occurs by bite of infected tick (vector). Infected tick, organism may be transmitted to tick offspring by transovarian method.
Virulence Factors
1. LPS (endotoxin) 2. Produce factors inducing phagocytosis. Inside phagocytes the organism survives & enters into the host endothelial cells. Evade host cell lysis. 3. Produces phospholipase A (lecithinase) which lyses phagosomes enabling rickettsia to enter into host cell cytoplasm (also deacidify vacuole)
Associated Diseases
1. Rocky Mountain Spotted Fever (RMSF): Systemic inf. following a tick bite (tick saliva). Rickettsemia causing vasculitis of the capillary beds of many organs particularly of the lungs & skin producing a fulminant disease. Symptoms: - rapid onset, high fever, nausea, vomiting, myalgia, headache see macular rash Rash spreads from extremities to trunk. (rash works inward) Disease may lead to pulmonary failure, renal failure, encephalitis, coma, & death.

Ab may be important initial barriers against inf. Previous inf. confers longlasting immunity.
Oral do Oral doxycycline Pregnant women are treated w/ chloramphenicol Prompt removal of ticks also important as preventive measure.
Mnemonic vect/spec/dis Ricky-ticky spot Caus. Agent: Rocky Mount. Spotted Fever (RMSF) #1 rickettsia disease & nonvector borne disease in US pop. Also note: Ticks may deliver Rickettsia or lyme disese
non-motile aerobic OBLIGATE INTRACELLULAR PATHOGEN
Has to be attached 24-48 hr in order to become encouraged w/ blood & to transmit the organism to man.
4. Organism is able to survive in rat blood & flea feces 5. Slime layer
Test Question: #1 non-vector borne disease in US Rocky Mountain Spotted Fever primarily found on East coast Test Question: #1 vector borne disease in US Lyme disease (carried by tick)
Spirochetes (cork screw)

-
outer most layer is referred to as an outer sheath (glycosaminoglycan) underneath is the outer membrane (peptidoglycan, lipids + covalently linked proteins) encase the periplasmic space where endoflagellae are located directly underneath the periplasmic space is inner membrane (cytoplasm) Cytoplasmic tubules (body fibrils) NO LPS Has a layer of peptidoglycan
Chlamydia
-
Gram (-), obligate intracellular organisms w/ unusual life cycle NOT spirochetes!!! Obligate intracellular parasites !!! Can not synthesize ATP! o No cytochromes or flavoproteins. Cant metabolize glucose to pyruvic acid using pentose phosphate pathway
Test Question: Endoflagella (axial filaments) inside of outer membrane NOT exposed to outside but can be shed in infected individual. Lives in intestines & in mouth
a) Non-specific blood tests: (agglutination) indicate present infection, since individual become (+) upon infection but levels decrease during chronic disease. Tests for Syphilis 1. Complement Fixation (Wasserman) indirect test: used to detect presence of reagin antibodies (reagan is antibodies directed against cardiolipin) Cardiolipin is an antigen which is released by damage host cells & present on the treponeme. 2. Rapid Plasma Reagin (RPR): also a reagent cardiolipin & is a carbon agglutination test 3. Venereal Disease Research Lab (VDRL) test: Cardiolipin + serum, check for clumping (means + results of antibodies against cardiolipin) AKA Flocculation test 4. Treponemal Specific Blood tests 5. Fluorescent treponemal antibody Absorption test (FTA-abs) 6. T. pallidum Hemagglutinin Assay (TPHA) Vocabulary Disease Symptoms: 1. Charcots disease: trophic degeneration of knee joint. Loss sensation due to neurosyphilus 2. Condyloma: fusion of 2nd syphilitic lesions around the anal areas 3. Gummata: ulcerous skin lesion (chewy gum) 4. Hutchinsons teeth : teeth are translucent. Incisor-like 5. Saber shins: affects long bones 6. Saddlenose: perforated nasal septum 7. Tabes dorsalis: destruction of dorsal roots of spinal cord
Serology
Chlamydia Life Cycle: 1. Small dense cell: ELEMENTARY BODY (infectious form but NOT replicating) it is outside of the host. Enters the host via phagocytosis DNA:RNA, 1:1 ratio = infectious particle 2. Next 8 hr, elementary body reorganizes into large, less dense cell called reticulate (or initial) body 3. Reticulate body: (this replicates) , grows in size & divides by binary fission (DNA:RNA ratio is 1:4) this is NON-INFECTIOUS form 4. 24-48 hr, reticulate bodies reorganize into dense elementary bodies & developmental cycle is complete when host cell liberates the small dense infectious cells.
Cell Features
Treponema pallidum Thin (0.5 u) tightly coiled spirals (5-15u) g(-) difficult to see b/c too thin Visualized w/ darkfield microscopy! or immunofluorescent microscopy & silver impregnation Moves using axial filaments, ENDOflagellae Microaerophilic Sensitive to environmental influences
Colony Features
Can not be cultured in vitro!!! Grows in rabbit testicles or in rabbit epithelial cell culture
Lab Charact.
Look for spirochetes using direct miscroscopy Darkfield & immunofluorescent methods & SEROLOGY

Man is only reservoir. Horizontal transmission by sexual contact. Vertical transmission (mother to child) through the placenta in utero. Highly infectious! Less than 10 spirochetes to cause disease!
Virulence Factors
1. Glycolipid instead of LPS (Glycolipid is rich in cardiolipin & other phospholipids to test for syphillus) 2. Motility 3. complex outer membrane structure w/ few membrane bound outer proteins 4. Outer membrane promotes adherence to host cells by tips bacteria 5. Hyaluronidase: enables spirochete to invade host tissue 6. Survive intracellularly (phagocyctic cells) & extracellularly in host 7. fibronectin (antiphagocytic) blocks phagocytosis
Associated Diseases
Syphilis (3rd most common STD) 1. Primary syphilis: systemic inf following sexual contact. Typically hard, painless chancre forms site of entry (genitals, mouth or anus) w/ spirochemia (spirochetes in blood stream) Sympt. 4-6 weeks. Most contagious stage. May see > 1 chancre in AIDS patient. 2. Secondary syphilis: persistent spirochemia, 3 weeks 3 months. Papular rash develops entire body. Spreads from trunk to soles, genitalia, & mucous surfaces. AKA Great Pox (Great Imitation) w/ fever & soar throat. Spirochete may invade any organ of body. Rash may last up to many months. Contagious. Organism may be isolated from rash. May develop LATENT disease. Condylomata (bacteria continue to multiply & deep-seated lesions) 3. Tertiary syphilis (LUES) NOT CONTAGIOUS! Disease affect any organ, may re-occur. T. pallidum, only observed in the CSF. Lesions on tongue, gummata lesions, & other effects on skin, bones, & blindness & Charcots knee 4. Congenital syphilis: transplacental inf. of fetus at 12 latent stages in mother. Death of fetus (blindness or deafness). Also: saddle nose, saber shins, skin rash, Hutchinsons teeth, heart malformation, & liver damage.

IgG and IgM develops by end of 2nd stage are important. Immunity takes a long time to develop in part b/c so there are few proteins on surface of T. palladium. Little protection immunity during 1 and 2 stages. T cells are involved in gumma f(x)
Syphilis is treated w/ penicillin (at all stages) & penicillin can also be given prophylactically. If sensitive Pen. Use ==> erythromycin or tetracycline
Cell Features
Leptospira Interrogans g(-) spirochete thin tighly coiled spirals w/ unusual hooked ends Use darkfield microscopy, immunofluorescent miscroscopy or stained by Silver impregnation technique. Obligate aerobe Motility (via 2 endoflagellae but least motile of all spirochetes) Interrogans: shape, question marks ??? complex outer membrane structure contains LPS
Colony Features
Can be cultured in vitro. Grows rapidly in complex media Uses fatty acids & alcohols as carbon source. Likes alkaline conditions.
Lab Charact.
Serological tests such as agglutinating complement fixation or lysis in presence of complement. Culture from blood, CSF, & urine.

Parasites of non-human animals (ie livestock & dogs). Best friend (dog prone to infect man) Animal kidneys are resvoir. Eating kidney, or consuming water contaminated w/ animal urine. Zoonotic infection Survives for months in soil & water but sensitive to Chlorine
Virulence Factors
1. LPS (endotoxin) 2. Hyaluronidase - invasiveness 3. Outer surface 4. Maybe hemolysin 5. Motility & thinness (penetrate intact mucous membranes; skin via small cuts or abrasions)
Associated Diseases
Severe case: (effect liver & kidney) LEPTOSPIROSIS which is usually a biphasic disease. Moves quickly & effects blood. a) Leptospiremic phase: presence of leptospires in blood & CSF. Abrupt onset of fever, shaking chills, headache, & myalgia. b) Immune phase: Accompanied by IgM production. Aseptic meningitis (no bacteria in blood but effects brain) . Onset of hepatic & renal failure & widespread hemorrhages & shock. Also known as Weils Disease due to an autoimmune response causing liver damage b/c of molecular mimicry. AKA INFECTIOUS JAUNDICE (yellow/green liver) . Has 2 phases: 1. Anicteric phase: w/o liver 2. Icteric phase: w/ liver involve

IgM & IgG are important Autoimmune response may be involved in disease process
Oral doxycycline, erythromycin, or penicillin
__________ * Twitch motility differs from spirochetes
Lyme disease Borrelia burgdorferi #1 vector borne disease US
Cell Features
Thin Loosely coiled long spirals (spirochete) g (-) Use darkfield microscopy, fluorescent miscroscopy + acridine organe dye or stained by Silver impregnation technique. Microaerophilic Rotational motility (endoflagellae, axial filaments) DNA is fragmented w/ some being linear
Colony Features
Cultured in vitro Grown on BarbourStoennerKelly medium contains bovine serum albumin (BSA) & rabbit serum at 30C
Lab Charact.
Darkfield microscopy Use ELISA Western blot also PCR

Primary reservoir is the mouse including white food mouse, dusty footed wood rat, chipmunks, and DEER. Vectors are the primarily Ixodid ticks
Virulence Factors
1. Glycolipid (similar to Treponema) NO LPS 2. Surface protein: produces many different surface antigens during infection. ANTIGENIC VARIATION 3. penetrate epithelial cells 4. Survives in blood & in tick ability to resist phagocytosis 5. Hemolysin
Associated Diseases
LYME DISEASE: > 1 stage Stage 1: appears - Erythema Migrans (EM) or Erythema Chronicum Migrans: Lesion or rash (Bulls eye lesion) - Symptoms: headache, fever, stiffneck, malaise, & lymphadenopathy. Stage 2: - Lyme arthritis (uniarticular ie involving 1 joint) Reversible w/ treatment. - Symptoms: neuroborreliosis (meningitis, peripheral neuropathy, encephalitis, Bells Palsy) may last for months years Stage 3: Follow a latent & asymptomatic period. Late or Chronic Lyme disease. Symptoms: similar to stage 2 but worse. Mostly arthritis.

IgG and IgM against outer surface antigens (Osps) important but undergo antigenic variation.
Stage 1:
Oral doxycycline
Stage 2 & 3: IV ceftriaxone Prevention Tips Dress properly w/o skin exposed, use insect repellent
Infection of man occurs by tick bite & transfer of organism during tickengorgement! Transmitted in vector by transovarian route. Also tick saliva or deposition of feces into wound.
Cell Features
Borrelia recurrentis relapse fever Epidemic Thin Loosely coiled long spirals (spirochete) g (-) Use darkfield microscopy, fluorescent miscroscopy + acridine organe dye or stained by Silver impregnation technique. Microaerophilic Rotational motility (endoflagellae, axial filaments) DNA is fragmented w/ some being linear
Colony Features
Cultured in vitro Grows slowly on complex at 30C
Lab Charact.
Darkfield microscopy

Humans are believed to be only reservoir (epidemic form of disease). Vectors for the epidemic organism are lice (therefore, louse-borne disease) Endemic form of disease is found in animal & human reservoirs & appear to be spread by ticks.
Virulence Factors
1. Glycolipid 2. Surface protein (VARIABLE MAJOR PROTEIN) which produces many different surface antigens, resulting in several relapses (ANTIGENIC VARIATION). 3. ability to penetrate epithelial cells 4. Survives in blood & in lice has the ability to resist phagocytosis
Associated Diseases
Relapsing Fever: > 1 stage Stage 1: 1st fever symptoms (maybe fatal due to shock-hypotension). Spirochetes from lice (or tick) penetrate the skin & skin & spread through the blood. Treat w/ antibodies will clear most circulating organisms, so host experience a non-febrile latency period 7-10 days. Stage 2: Spirochetes go through antigenic variation & a new variant will be produced. Results in bacteremia & a second fever stage (relapse).

IgM & IgG against outer surface antigens are important leads to complementdependent lysis. Cytokines may be involved in disease resolution
Oral doxycycline Penicillin Tetracycline Chloramphenicol Erythromycin (children & pregnant women)
NOT spirochetes! Chlamydia trachomatis
Cell Features
g (-) does not have typical cell wall of peptidoglycan but sensitive to Penicillin compact inclusion body w/ glycogen, make folic acid therefore sensitive to sulfonamide ONLY!!! (differs from . C. psittachi)
Colony Features
Grows in cell culture
Lab Charact.
Difficult to diagnose. LGV test dead bacteria injected under skin & look for DTH. Serology 15-20 different serotypes

Humans are reservoir. Infection of man occurs by sexual contact & by autoinoculation to other parts of body. Mother to child transmission is possible at birth. Maybe transmitted by direct contact with fingers, contaminated towels & clothing. Can be transmitted sexually to other adults leading to genital symptoms. Can be spread by fingers, towels, clothing can even spread in chlorinated water (swimming pool conjunctivitis)
Virulence Factors
1. Intracellular survival a) stimulates nonphagocytic epithelial cycle to engulf them b)Inhibit phagosomelysosome fusion (all 3 chlamydia have them!) 2. Unusual life cycle: elementary bodies can infect host macrophages & epithelial cells, becomes reticulate bodies & produce new elementary bodies ==> released when host cell lyses. 3. Endotoxin 4. toxic factor 5. Type III Secretion system
Associated Diseases
Male STD: most common STD in US. Urethritis involve urethral discharge. (SYPMTOMATIC) Female STD: Cervicitis, endometritis, PID involve discharge. May cause sterility women are ASYPMTOMATIC Swimming Pool Conjunctivitis: Spread by fingers, fomites & even chlorinated water into eye. ADULT INCLUSION CONJUCTIVITIS: STD TRACHOMA: Chronic eye inflammation by infecting eye. Lymphogranuloma venerum:, (LGV): develop into buboes and lead to elephantiasis of genitalia & rectal structures as result of perirectal scarring. Neonatal infection: Due to vaginal passage can cause disease by either being aspirated into lung or by conjuctiva of neonate. a) Infant atypical pneumonia: - long term complications & otitis media b)Inclusion conjunctivitis: may have similar to trachoma Reiters Syndrome: Arthritis, periostitis on calcaneus (heel) pain AKA Lovers Heel

Ab not effective. PMN effective in killing.
Oral doxycycline
Sulfonamide (unique) Erythromycin Cefoxitin & doxycycline if concurrent w/ N. gonorrhea infection Antibiotics such as erythromycin or tetracycline are used in form of eyedrops for new borns.
Most common STD
NOT spirochetes! Chlamydia psittaci (psittaci) Parrot Fever
Cell Features
g (-) does not have typical cell wall of peptidoglycan but sensitive to Penicillin diffuse inclusion body no glycogen cant synthesize folic acid, resistant to sulfonamide!
Colony Features

Contact w/ parrots & other psittacine birds can spread to other animals (cattle, swine, cats, dogs) Can get into: environment from feces & survive a long time !
Virulence Factors
1. Intracellular survival: a) stimulates nonphagocytic epithelial cycle to engulf them b) inhibit phagosomelysosome fusion (all 3 chlamydia have them!) 2. Unusual life cycle: Elementary bodies can infect host macrophages & epithelial cells 3. Endotoxin similar to LPS 4. Toxic factor 5. Type III secretion system
Associated Diseases
Psittacosis (ornithosis) PARROT FEVER: Can exist as asymptomatic, likely to be severe, frequently fatal pneumonia. Can involve other organs: jaundice, acute thyroiditis, meningitis w/ delirium. It is a latent infection. Lung inhaled form it is atypical pneumonia. Spread by human to human.

Ab not effective. PMN very effective in killing. Previous infection provides no immunity & subsequently see relapse & reinfection.
Doxycycline and azithromycin Alternatives: Ofloxacin, erythromycin, amoxicillin (pregnant women) Quarantine imported birds
NOT spirochetes! Chlamydia pneumoniae
Cell Features
g (-) does not have typical cell wall of peptidoglycan but sensitive to Penicillin diffuse inclusion body no glycogen cant synthesize folic acid, resistant to sulfonamide!
Colony Features

Humans are reservoir. Occurs in respiratory droplets. Epidemics are possible TWAR strain caused acute respiratory disease.
Virulence Factors
1. Intracellular survival: a) stimulates nonphagocytic epithelial cycle to engulf them b) inhibit phagosomelysosome fusion (all 3 chlamydia have them!) 2. Unusual life cycle: Elementary bodies can infect host macrophages & epithelial cells 3. Endotoxin similar to LPS 4. Type III secretion system
Associated Diseases
1. Atypical pneumonia: (sneezing or coughing): mild or asymptomatic but in elderly, it can be fatal. Involves in the lower lobe. Pneumonia and bronchitis in adolescents & adults is often seen w/ pharyngitis and sinusitis. Other Symptoms: nonproductive cough, fever, chills, headache & malaise. Complication of coronary artery disease & endocarditis.

Ab not effective. PMN very effective in killing. Previous infection provides no immunity & subsequently see relapse & reinfection.
Doxycycline and azithromycin Alternatives: Ofloxacin, erythromycin, amoxicillin (pregnant women)
Mycology (Fungi)
Characteristics: Eukaryotic cells w/ cell walls (no peptigylcan) o Chitin, cellulose, glucans, mannans (ex. polymers of sugars) o Non-photosynthetic, Heterotrophs, saprophytes, or saprobes, parasites Cell membrane o Ergosterol o No motility Cryptocococucus neoformans (only one with capsule), anti-phagocytic! 2 forms: a) unicellular yeast (chains) b) multicellular mold (septate) (filaments structures aka hyphae) Coenocytic: several nuclei present in cytoplasm of 1 cell (multinucleated) Mat of hyphae = mycelium or thallus Vegetative hyphae = penetrates substrates for nutrient acquestion Reproductive hyphae: aerial structures for reproduction
Zygomycetes: (phycomycetes): ex. bread molds, most primitive, filaments, aseptate, sexual & asexual (sporangium formation) Ascomycetes (Ascomycotmia): Asexual - conidia Sexual - ascospores (incl. dermatophytes) and spherules
Basidiomycetes: septate hyphae, sexual spores Deuteromycetes (Fungi Imperfectii) has sexual stages Culture Fungi: Sabouraud agar o Slightly lower pH (more acidic) o Contains dextrose & peptone o Chloramphenicol to inhibit bacteria o Cyclohexamide (Acti-Dione) inhibit saprophytes Molds grows away from plate, looks fuzzy o Vegetative hyphae = roots Yeasts creamy opaque colonies Dermatophyte Test Medium (DTM) inhibits bacteria cyclohexamide to inhibit saprophytic molds dermatophytes turn medium yellow ==> red Corn-meal Agar test for spore formation visualize chlyamydospore & blastocondia production candida albicans Monomorphic fungi dermatophytes o E (NS) o M (SH) o T (NSH) Cryptoccous neoformans (encapsulated, endosporulating, spherules) Aspergillus fumigatus (fungus ball) Dimorphic fungi Histoplasma (dusty environment, bird feces) blastomyces (valley fever) coccidiodies sporothrix (rose garden cuts)
c)Dimorphism triggers: 1) 25C ==> forms macrocondia (mold), Chlamydia spore 2) 37C ==> budding yeast form a non-mold form (C. immitis) d)Reproduction: Anamorphic - Asexual Telomorphic - Sexual
Sexual form NOT identified: (Fungi Imperfectii or deuteromycetes) 99% of ASEXUAL spore o Fragmentation o Fission (equal size) o Budding (new buds, vary in size) o Spore formation: mostly budding o Yeasts: fission, budding Spores produced in sac sporangium w/ spores sporangiospores
Thallospores: arthrospores: barrel shaped, thick-walled produced by hyphae fragmentation chlamydospores: swelling of hyphal fragment, thick double wall blastospores: simple budding from parent cells Sexual Reproduction (cells are 2N), Perfect state oopspores zygospores ascospores (sac) basidiospores: club shaped (mushroom)
Lab diagnosis: Potassium hydroxide: (KOH) used for diagnosis + heat for ID Calcofluor: fluroscent stain, UV microscope Gomori methenamine silver stain (GMS): tissue stains red & fungus blue Lactophenol cotton blue dye: (stain hyphae): aniline stains fungal India ink & test for capsule (-) stain ==> cryptoccocus neoformans 3 types of transmission: Anthropophilic ==> human to human Zoophilic ==> animal to human, ex. Microsporum canis Geophilic ==> soil to human, ex. microsporum gypseum Candida pseudohyphae, burrows into tissue yeast disseminate easier body via blood Antifungal agents: (ex. Nystatin, Amphotericin B) Polyenes: creates large pores in fungal cell membrane by binding to erogsterol Azoles: ex. ketoconaxole, fluconaxole, itraconazole, inhibit ergosterol, block cytochrome P450 enzyme Allylamine: ex. naftine, binafine, terbinafine, lamisil o tolinaftate : ex. tinacitin ==> ergosterol Griseaans : inhibit microtubule so cells do not divide Potassium iodide (KI) : antifungal therapy to treat sporothrix schenckii infection Mycotic Infection: cutaneous superificial subcutaneous systemic CUTANEOUS INFECTION (Dermatophyte infection): Dermatophytes: invade keratinized & cutaneous areas produce keratinase, collagenase, elastase affect stratum corneum (skin) grown best at 25C not invasive Tineas (ringworm) Tinea Capitis (scalp) itch on scalp w/ 3 patterns Caused by microsporum species (M. canis, use Woods light) o Endothrix: inside hair shaft o Ecotothrix: outside hair shaft o Favic: hyphae arthoconidia & air bubbles form inside hair Honey comb pattern
Tinea Corporis (non-hairy parts of body) mistaken for lupus scaly popular eruptions Tinea Pedis (Athletes foot) public showers, swimming pools, watery lesions btw toes, show peeling & cracking of skin caused by: Trichophyton rubrum & T. mentagrophytes Tinea Favosa (form of scalp) yellow, cap-shaped crusts looks like a honey comb T. Schoenleinii (fluoresces yellow-green) Tinea Unguinum (nails - infection) superificial, only pits of nails involvement of nail surface w/ invasion beneath nail plate onychomycosis (nail infection) caused by non-Dermatophytic o saprobe fungi ex. Aspergillas Fungal finger nails ex. car wash workers, common cause Candida Albicans Tinea Cruris (Jock Itch) can be epidemic form w/ exchange of clothing, towels, scaling lesions, itchy & often dry Dermaphytids not grown on Sabouraud allergy response w/ dermatophyte infections IDs (severe itching especially after antifungal agent) Fungal organism NOT present Epidermophyton (NS): thermally monomorphic, no microconidia but macroconidia, cigar shape Microsporum (SH) thermally monomorphic Trichophyton (NSH) thermally monomorphic
Trichophyton (NSH) Thermal morphic moid Cell features Mentagrophytes Yes Septate hyphae, spiral, microconidia, grape-like cluster Rubrum Yes Septate hyphae, oval, tear-drop, peg-shaped, cigar shaped Bright RED* Tinea Capitis Tinea Corporis Tinea Cruris Tinea Pedis Tinea Ungium Onychomycosis Scraping of infected skin, nail, KOH Tonsurans Yes Various size & shape microconidia w/ large spherical conidia Black dot Black spores lead to tinea capitis
Diagnosis Disease
Malassezia furfur & M. Ovalis (Pityrosporum ovale) Dimorphic & long hyphae Comes from furfaraceous or scaly Cell feature - yeast like cells - hyphae are usually absent - spaghetti & meatballs Dxn Disease - Superficial inf. Of skin (Tinea Versicolor, Pityriassis Versicolor) - skin-inf. non-itchy, scaly, pale spots on shoulders & back, chest, & upper arms! Treatment Woods Light, orange-red fluorescent hyphae Piedraia Hortae dark/black hard nodule hair shaft (Black Piedra) Disease - Base of the hair to fall out Trichosporon Beigelii (T. aschii, T. mucoides, T. inkin) baige associated w/ white Piedra Disease - Superificial infection of hair roots
Dxn
Microscporum Gypseum Complex (M. Canis & M. Audouinii) thermally monomorphic mold Cell feature - Septate hyphae - microconidi, along the hyphae & club shaped Dxn - KOH, non-treated test w/ sabouraud agar for microsporum canis use woods lamp (yellow-green) fluorescence Disease - Tinea capitis - Tinea Cruris - Tinea Pedis Transmission - dog ==> human (zoophilic) & geophilic transmisin Treatment - affected skin, kept cool & dry - apply topicl antifungal agents (cream) - tinea capitis ==> oral griseofulvin - Lamisil Hortaea Wereckii = Exophiala Werneckii : Dematiaceous fungi or pigmented fungi o Non-invasive o Pigmented (b/c melanin production) Disease: o Produce superificial inf. of skin, Tinea Nigra (black growth on skin) but non-invasive o Skin infections, non-scaly, smooth, brown-black painless spots
SUBCUTANEOUS INFECTION (Dimorphic) stays localized Sporothrix Schenckii (Gardeners w/ hay, rose bushes, ferns) puncture of skin thermally dimorphic yeast-like fungus dematiaceous daisy clusters Cigar shaped budding yeast (37C) Wrinkled round brown, black colonies Infectious occurs (scratches, punctures) during gardening from wood, splinters, Prevelant in South US Zoonotic transmission: armadillo & infected cats Disease - painless nodules forming along lymphatic channels Treatment Potassium iodide Madurella Spores thermally monomorphic molds, dematiaceous true fungal infection, brown-colored Disease fungal mycetoma (Eumycetoma) madura foot, resembles nocardiasis (actinomycetoma) Treatment - difficult to cure
SYSTEMIC INFECTIONS: (Inhales into lungs) ALL thermally dimorphic True, frank, primary pathogens Via respiratory rate (inhaled spores) Blastomyces dermatitidis: yeast like fungus, looks like figure 8s multi-nucleated, forms granules of skin no cell wall, bird droppings Mississippi river to East coast Dxn - multi-nucleated budding yeasts, single broad-based 888s Disease NAmerica blastomycosis (mild pulmonary inf), skin lesion Formation of granulomas of skin & bone Paracoccidiodes brasiliensis: - thermally dimorphic yeast-like fungus - UNINUCLEATE!, multiple budding mother cell w/ buds having narrow bones - Cause systemic infection, more mucosal surface - Found mostly in S. America blastomycosis (granulomatous spreads to lungs to other mucous surfaces of nose, mouth, & GI tract) -Looks like ships wheel, steering wheel, pilot wheel - endemic Coccidioides Immitis (C.Posadasii) dimorphic fungus: changes form to spherule at at 37C Cell feature terminal arthrospores attached directly to hyphae spherules in tissue specimens, barrel shapped! Transmission direct inhalation (mold spores, arthrospores) from soil & dry climates Southwest US (Central or S. America) likes Nitrogen associated w/ bird droppings (feces) Disease Coccidiomycosis, highly infectious disease flue-like pulmonary infection, CNS (Meningitis)!!! Leads to erythema nodosum (DTH response, red tender nodule on skin) Desert rheumatism San Joaquin Valley FeverCali ID test looks for DTH response Histoplamsa Capsulatum Var. Capsulatum: dimorphic yeast-like fungus & small oval microconidia spiny macroconidia attatched to hyphae, knobby (tuberculate macronidia) Transmission - direct inhalation of small molds (microconidia) from soil or bird droppings. They are spiny & knobby looking! - Mississippi + endemic, Ohio River, S. America, & Africa Disease - Most common respiratory mycotic inf pneumonia, granuloma - reticuloendothelial system (RES) found intracellularly w/in macrophages. Like at TB test can use DTH - Chronic disease: reactivation enlarged granuloma, liver, spleen
OPPORTUNISTIC INFECTIONS: (Colorized, immunocompromised state of host) Aspergillus fumigatus: thermally monomorphic mold inhale spores immunocompromised patients Fungus ball (aspergilloma) spore germinate (Farmers Lung) HAY FEVER!!! A. Flavus produces aflatoxin potent liver carcinogen. INVASIVE!!! Candida Albicans: Dimorphic but NOT thermally but grown on corn-meal produce pseudophyae Use as diagnositic: Germ tubes test (true hyphae) this is a unique feature! Part of normal flora (FurFur & tricosporum???) Produces ==> chlamydospores are unique to this candida cream-colored pasty colonies Transmission - normal commensals of human & animal GI, resp, tracts skin & female genital tracts Disease ORAL THRUSH: (AIDS immunocompromised) - produce white patches in mouth & tongue continue to GI tract Cutaneous candidiasis: diper rash INTERTRIGINAS CANDIASIS (Intertrigo): - appendages immersed in H20 long periods, moist parts in diabetes ONYCHOMYCOSIS: nail inection VAGINITIS: (Moniliasis): vaginal infection of women Chronic Mucocutaneous Infection: - CMI failure (T-cell deficiencies) infection associated w/ skin, oral mucosa, respiratory mucosa, GI & GU mucosal surfaces - antibiotics Treatment Cryptococcus Neoformans: capsule, visible w/ India ink thermally monomorphic yeast capsule is anti-phagocytic Cell feature - oval shapped Dxn - Mayers stain to see PINK capsules - CSF sample prep. w/ 10% KOH & India ink Disease - result in cryptococcosis (pulmonary infection) - to meninges & brain thrives on CSF (Meningitis) - occurs often immunocompromised - can be unrecognized or asymptomtic Transmission - Via inhalation of yeast found in soil & pigeon droppings Treatment - Ampotericin B & Latex agglutination! Mucormycosis (Phycomycosis or Zygomcosis): mucor, absidia, rhizopus species invades tissues, brain (nasally) it is a bright mold! Cell feature aseptate or coenocytic & invasive member of Zygomycetes (phycomycetes) sporangia form at 90 degree angle from hyphae
INDI Organisms # 4 Virus Size & Structure 20-300 nm size (picornavirus ==> poxvirus) appears spheres or rods Contain either DNA or RNA, NOT both! All have a protein coat, capsid (repeating capsomers) o Capsid could is outer surface o Others could have lipoprotein envelope composed of phospholipids bilayer Enveloped: picked up from nucleus or p.membrane or created from cytoplasm ether sensitive Composed of nucleic acid & capsid protein is called nucleocapsid Shape: spherical (icosahedral) or helical symmetry o Exception: poxvirus looks like a brick shaped (complex) All human viruses have helical nucleocapsid are enveloped No naked helical viruses infect humans. Icosahedral nucleocapsid can be either enveloped or naked Viral Nucleic Acids Retroviruses: have two copies of genome (diploid) DNA Viruses o Are dsDNA except parvovirus o Are icosahedral, except poxvirus (brick, complex shaped) o Replicate their DNA in nucleus, except poxvirus Virus Family Parvovirus Papovirus Adenovirus Herpes virus DNA type ssDNA dsDNA circular dsDNA linear dsDNA linear dsDNA linear Virion (associated polymerase) No No No No Envelope Naked Naked Naked Enveloped (nuclear) Enveloped DNA replicates in: Nucleus Nucleus Nucleus Nuclues; virus assemble in nucleus Cytoplasm (DNA dept RNA polyermase) Nucleus, RNA intermediate Major viruses B-19 Papilloma Polyoma Adenoviruses HSV: VaricellaZoster, EBV Variola Vaccinia Molluscum Contagiosum Hep. B
Poxvirus
Yes
Hepadnavirus
Yes Partially dsDNA circular Mnemonic: Parvas Papa Adds Her Poxes to Hepas
Enveloped
(+)RNA Viruses Virus Family Calicivirus RNA structure ss(+) RNA Linear Non-segmented ss(+) RNA Linear Non-segmented Virion (associated polymerase) No polymerase Envelope Naked Shape icosahedral Multiplies cytoplasm Major viruses Norwalk agent hepatitis E Polio, Enteroviruses Rhino Coxsackie Hepatitis A Yellow fever, dengue, St. Louis encephalitis Hepatitis C Rubella, WEE, EEE, Venez encephalitis Cornoavirus
Picornavirus
No polymerase
Naked
icosahedral
cytoplasm
Flaviviros
ss(+) RNA Linear Non-segmented
No polymerase
Enveloped
icosahedral
cytoplasm
Togavirus
ss(+) RNA No polymerase Linear Non-segmented Coronavirus ss(+) RNA No polymerase Linear Non-segmented RNA dep. Retrovirus Diploid DNA ss(+) RNA Polymerase Linear Non-segmented Mnemonic: Call Pico and Flo To Come Rightaway
Enveloped
icosahedral
cytoplasm
Enveloped
Helical
cytoplasm
Enveloped
Icosahedral or truncated conical
Nucleus
HIV, HTLV, Sarcoma
Papovaviruses: group of DNA viruses that produce benign & malignant tumors virus types: o Papilloma: HPV types 1-58+. Causes human, cat, dog, & rabbit warts o Polyoma: found in mice which are asymoptomatic. If induced into newborn animals results in malignant tumors virus structure: o icosohedral capsid virion, dsDNA, circular, replicated & assembled in nucleus o p53 and RB regulates cell growth but papovaviruses binds to them to promote cell growth o T angitens regulates transcription with the p53 and RB, T antigen is found w/ viral DNA for replication to continue in cell. Papovaviruses: o Papillomaviruses replicate in the squamous epithelium of skin & mucous membranes to produce warts o Skin warts, anogenital warts (cervical cancer, 16,18 where E1 & E2 become inactivated so that E6 binds to p53 & E7 w/ RB) Koliocytosis: infectious human papillomavirus of epi layer of uterine cervix or external genitals (condylomata acuminata) Hyperkeratosis: inflammation w/ excess growth of prickle cells of skin Treatment warts: o Remove surgically cryotherapy (liq. N2), electric, or chemical means (ex. podophyllin) o Laryngeal warts: remove surgically but NOT w/ irradiation b/c could induce malignant changes o Imiquimod + IFN can promote faster healing applied to topically (ex. external genital regions) o Cidofovir : antiviral nucleoside inhibits viral DNA polyermase Adenovirus: Virus structure: o dsDNA, naked, icosahedral, linear shaped, fiber (attachment protein + hemagglutinin activity) o 47 different types, permissive, found in human adenoids & tonsils Important misc facts: o Associated with conjunctivitis, GI tract, and upper respiratory disease (common cold). o Produce tumors in baby hamsters but NOT in humans. o Most common infection of tonsils & adenoids in early child life is from adeno types 3 & 7 and is latent. Parvoviruses The ONLY ssDNA, naked, icosahedral, linear, e-nucleated w/ mature RBC non-defective defective replicates only in multiplying host cells requires helper virus (Dependo virus) ex. of helper virus is (Adenovirusand Herpes Virus)
Disease: o Erythema infectiosum (fifth disease) - comment: remember a 5 finger slap in the face you get this redness! o 1 of 5 common childhood exanthems or rashes (looks like slapped cheek (facial rash) o Chronic hemolytic anemia (ex. sickle cell anemia) leads to aplastic crisis (lytic on RBC) o Immunodeficient can lead to chronic anemia transmitted: o vertically (cross placenta) results in spontaneous abortion associated w/ HYDROPS FETALIS
Herpesviruses dsDNA, enveloped, icosahedral, linear shaped, tegument : contains viral proteins & enzymes involved in initial replication Lab diagnosis: o Tsanck smear (scrapings of infection) see Cowdry Type A cells (acidophilic intranuclear inclusion bodies) see syncytia Virus replication: o Virus induces synthesis of viral thymidine kinase & DNA polymerase o Phosphonoacetic acid inhibits herpesvirus replication by inhibiting viral DNA polyermase o Viral protein are made in cytoplasm & enters the nucleus where they assemble w/ the DNA into virus particles o Virus buds from nuclear membrane, pickup lipid bilayer & viral proteins that have been inserted into it. o Infection can be lytic or lead to latent infection
Latent in nerves
Latent in leukocytes-WBC
- Herpes Type 1 & 2 ( HSV-1 & HSV-2) - Varicella-Zoster: a) chicken pox: (varicella portion) acute infection (children) b) shingles: reactivation of virus of chicken pox - Epstein Barr Virus (EBV) a) Burkitts lymphoma (tumor in jaw), nasopharyngeal carcinoma b) infectious mononucleosis
HSV-1 (usually infects above waist) - Location of latent: Trigeminal dorsal root ganglia - Acute herpetic gingivostomatitis: most common infection for Type 1. Gums swollen! Similar to herpes labialis. Oral herpes. Self-limiting. - Eczema Herpeticum:(Kaposis similar to Herp 8) infect fingers (herpes whitlow) - Keratoconjunctivitis: infects eye - Herpes labialis:(cold sores!!) NOT common cold, most common recurrent disease. - Encephalitis : residual neurologic defects
HSV-2 (usually infects below waist) - Location of latent: Lumbo-sacral dorsal root ganglia - Genital Herpes: lesions develop in genital organs. - Neonatal Herpes: transmitted to new borns - Aseptic meningitis :mild, self-limiting
Varicella-Zoster Chicken pox (multiple crops) - occurs in children via mucosa the upper respiratory tract - swelling of epi cells, eosinophilic inclusions found in nuclei of infected cells & end up attacking nerve cells - virus replication occurs in the nucleus - incubation time: 2-3 weeks - symptoms: fever, fash, vesicles appear - differs from small pox (1 crop)
Shingles - occurs in the posterior nerve & ganglia (Dorsal RG) - reactivation of the chicken pox - triggered by stress, immunocompromise, trauma
Treatment: o Acyclovir , vidarabine, idoxiuridine, trifluoridine Cytomegalovirus (Herpes 5) Latent in Leukocytes o Disease: Most infection of infants, caused by intrauterine or early postnatal infection (pass to child) Teratogenic: virus causes severe congenital anomalies in infants (mental retardation) Cytomegalovirus cells found in the epi tissues of liver, lungs, kidneys, lungs, GI, parotid gland, pancreas, etc. o Virus recovery: Virus can be recovered from the mouth, urine, liver, adenoids, kidneys & peripheral blood leukocytes Diagnosis of virus infection by owl cellsor owl eyes in the urine. Basophilic intranuclear inclusion body Also found in Conventional slow virus disease: involves brain infection o Treatment: Ganciclovir, foscarnet, cidofovir Vaccine is not effective
Epstein Barr Virus (EBV) latent in B cells are leukocytes o Disease: Burkitts Lymphoma & Nasopharyngeal Carcinoma Chromosomal translocation breakages are associated Associated with Kissing Disease (mono, results in large lymph nodes & spleen) Use Paul Bunnel test to detect mono WBC ex. Downey cells: B cells infected by EBV Herpes Virus 6: Lymphotrophic & ubiquitous associated w/ childrens disease Childhood exanthema subitum (roseola) Associated with multiple sclerosis Herpes Virus 8: Associated w/ Kaposis sarcoma, (found in Type I) problem w/ immunocompromised
Poxvirus Virus structure: o Largest DNA, enucleated, complexed shape Virus replication: o ONLY DNA replicates in the cytoplasm o Replicate in enucleated cells
Virus DNA and proteins are packaged into virus particles occurring in cytoplasm in the Guarnieri bodies
Small pox: o 2 variants, enters in the mucous membranes of upper respiratory tract with incubation of 12-16 days. o Virus multiplies in lymphoid tissues with infection throughout the body. May result in scaring. o Diagnosis: Incoluated in embyronated eggs o Treatment: cidofovir (inhibits DNA polyermase) also it is safer w/ less side effects Molluscum contagiosum o An ex. of a pox virus leads to skin infection, benign tumor, it is a nodular-wart-like growth o Transmitted: direct contact or fomites & spread by STD o Treatment: curettage (scrape) or liquid N2
Picornaviruses Enteroviruses (intestine) o Polio and coxsackie viruses Rhinoviruses (nose): common cold Cardiovirus: in rodents Virus characteristics: o (+)ssRNA, naked, icosahedral, smallest RNA virus, nucleic acid is infectious o Poliovirus: stable in acidic environment pH 3-9. Found in GI tract & in feces o Rhinoviruses: unstable in acidic environment pH 5-6. Found in oropharynx area o Replicates at 33C. Poliovirus o Smallest RNA, 3 serotypes (1-3): 1&2, 2&3 cross react, 1 & 3 doesnt cross react o Inactivated by UV, drying. 1M MgCl2 thermally stabilizes b/c of the capsid proteins. o Immunological properties: C antigencity is the empty capsid which lacks the vRNA. NO VIRUS RNA D antigencity: is the native complete virus HAS VIRUS RNA o Host: man is the ONLY natural host o Virus replication: adsorption (complete particles) ==> penetration ==> uncoating ==> translation (replication) ==> synthesis of vRNA ==> maturation ==> release o Disease: Starts oral route. Multiples in tonsil, lymph nodes, Peyers patches in SI. Asymptomatic shedding Infection Ingested virus Alimentary phase Oropharyngeal, virus in throat, intestinal mucosa Lymphatic phase Tonsils, deep cervical lymph nodes, virus in feces, peyers patch, Viremic phase Blood Neurological phase CNS, extraneural tissue, regional nerve ganglia o Infection: 90% in oropharnyx region Abortive: most common form. Malaise, fever, drowsiness, headache, nausea, vomiting constipation, & sore throat. Nonparalytic: asceptic meningitis similar to symptoms from abortive with stiffness & pain in back & neck. Paralytic poliomyelitis: flaccid paralysis, uncoordinated, painful spasms on nonparalyzed muscles Factors alters the disease: fatigue, tonsillectomy incidence, pregnancy, age, steroids Lab diagnosis: CSF in leukocytes Treatment: aridone (binds to receptors change confirmation) Prevention & Control: Vaccine Salk Formaline Inactivation Virus Sabin Live Attenuated Virus - grown in monkey kidney - grown in human diploid cells in culture - inactivated could induce polio - given orally: IgA - boosters needed 3-5 years - long term immunity - develops IgG & IgM - reverts to virulence - no herd immunity - herd immunity (virus cant spread, buffer zone)
o o o
Coxsackieviruses (enterovirus) o Coxsackie A: Found mostly in respiratory region. flaccid paralysis o Coxsackie B: Found mostly in the body region. spastic paralysis o Diseases: Nonspecific febrile illness: Can lead to polio-like paralytic disease Herpangia:fever, soar throat, anorexia, vomiting, abdominal pain, vesicles in palate, uvula. Self limiting. Not herpes! Pleurodynia: chest pain (Bornholm disease: Devils grip) Hand-Foot-Mouth: oral & pharyngeal ulcers which may spread to arms & legs w/ mild fever Mycoardiopathy: mycocardial disease in adults & children Common cold: upper respiratory infection Diabetes Melitis:abrupt onset of diabetes after infection w/ coxsackie o Control: Spread by feces, pharyngeal secretions, sewage Rhinoviruses o Virus characteristics:
o o
Common cold, at pH < 6-7 (unstable in acidic environment), found in nasopharyngeal cavity, not found in GI tract H&M strains Host: man Control: Vaccine is not possible b/c too many serotypes!
Coronarviruses Associated with common cold & SARS Virus structure: o (+)ssRNA virus, enveloped, naked, helical, lipid containing, 2 glycoproteins at its surface (E1 & E2 (activtes HA) Multiplication: o Different in sized viral mRNAs transcribed from vRNA o Occurs in cytoplasm: assembly by budding into ER & Golgi apparatus. Released by fusion via exocytosis o Multiplication is max. at ~32C Pathogenesis: o Aerosol and large droplets o Coryzas (swelling of mucosal membrane of oropharynx), sneezing, nasal congestion, etc o Some can cause gastroenteritis Prevention: o No vaccine or regulation available
Orthomyxoviruses (Myxoviruses) associated w/ the influenza Virus structure: o (-)ssRNA, enveloped, helical, segmented, own polyermase, infectious respiratory disease, 3 forms (A,B,C) o A type: replicate in humans & animals, B & C type: not as virulent Hemagglutinin (HA) - glycoprotein binds to cell receptors - main antigen against neutralizing antibody Neuraminidase ( NA) - removes sialic acid virus spread in respiratory tract Ribonucleoprotein (RNP) - code for structural & non-structural proteins - capsid, it goes into the nucleus
Virus replication: o Virus attach to receptor (HA) enters cell o pH change so fuses w/ membrane & release RNP o Viral polymerase cleaves host mRNA & uses capped primer to transcribe the vRNP. o mRNA & vRNA made in nucleus o HA & NA made in RER ==> SER until cell membrane & gets glycosylated o Virus made by budding from cell Antigenic shift Antigenic drift -b/c of high error of RNA polymerase - re-assortment - can have co-infection - can be pandemic - change in nucleic acid of virus Complications: o Associated w/ lung infection (pneumonia) Pneumonia: primary influenza, combined viral & bacterial, secondary bacterial pneumonia, Reyes syndrome: encephalopathy & fatty liver associated w/ Influenza B Associated w/ Guillain-Barre Syndrome: ascending paralysis Otitis media Treatment: Anti-viral - Amantadine hydrocholoride & rimantadine - Tamiflu - Relenza (works against NA - drug blocks uncoating (blocks replication) Vaccine Vaccine is prepared in eggs
Paramyxovruses Virus structure: o (-)ssRNA, enveloped, helical, non-segmented, HN and F proteins (2 spikes), contain RNA polymerase o F protein (fusion) causes lyses of rbc when mixed w/ virus Replication: o Synthesis of mRNA & proteins occur at the cytoplasm o HN & F proteins are assembled in the cell plasma membrane Virus types: o parainfluenza types 1-5: Infects humans & non-humans o mumps: paramyxovirus o measles: morbillivirus o respiratory syncticial virus: Parainfluenzas:
Upper respiratory disease: fever, rhinitis, pharyngitis, CROUP syndrome (laryngoracheobraonch) (barking cough difficult to breath)
MUMPS Pathogenesis: o Asymptomatic o Acute onset of parotitis w painful swelling in salivary glands & transmitted in saliva & respiratory secretions o Forms multinucleated cells (F protein) causes fusion of several cells (syncytia formation) o May lead to male sterility because cant expand due to tunica albuginea o Stensens duct: parotitis Measles (Rubeola) Acute highly infectious disease: w/ rash & respiratory symptoms o 3C (cough, coryza, conjunctivitis) o Lacks neuraminidase o Kopliks spots: vesicles in the mouth. Appear tiny red patches w/ white specks on buccal mucosa o Measles can impair CMI (cell mediated immunity) Complications: o Subacute sclerosing panenceophalitis (SSPE) : latent in individuals, brain cells have nuclear & cytoplasmic includsions of measles ribonucleoprotein, slow virus o Herpes 6 (multiple sclerosis) Respiratory Syncytial Virus (RSV) o Blocks breathing respiratory tract of young children < year old causes bronchitis & pneumonia .produce syncytia. MMR is a live attenuated virus vaccine Reoviruses ONLY dsRNA , naked, icosahedral, 10 segments, double capsid Disease: o Rotavirus: affects children w/ diarrhea. Looks like wheel shaped. Can see genetic re-assortment (shift in orthomyxovirus Toga Virus (cloak) (+)ssRNA, enveloped, 3 proteins Rubella (German Measles) Rubivirus o Rubella virus: Transmitted by (starts in) respiratory tract. Highly infectious. Spread in blood. Symptoms: rash begins on face, low fever, enlarged lymph nodes & spleen. Congenital Rubella Syndrome: o Complications involve cardiovascular, hematologic, neurologic, opthalmlogic, osteologic, & auditory systems. o Mental retardation may occur o Teratogenic: CONGENITAL ANOMALIES Leads to spontaneous abortion MISC: T.O.R.C.H. To Toxoplasma R Rubella (German measle) TogaVirus C Cytomegalovirus & Coxsackievirus H Herpes Virus Rhabdovirus Virus structure: o bullet shaped, enveloped, made up of 5 proteins w/ 1-protein outside (glycoprotein G) o (-)ssRNA, helical, contains RNA polymerase o Cytoplasmic replication Rabies Disease o Infection of CNS of all warm blooded animals (mammals) o Transmitted via bite wounds with saliva Rabies multiplies in muscle & connective tissue at the infection. o 3 stages in human rabies: Prodromal phase: malaise, anorexia, headache, nausea, vomiting, sore throat, & fever. Excitement phase: salivation & perspiration. Hydrophobia (fear of water) b/c fear of swallowing due to pain Depressive (paralytic) phase: convulsive seizures, coma, and death Lab Diagnosis o Presence of Negir bodies in nerve cells. o Antibodies can be detected by immunofluorescence, complement fixation, or neutralization. Immunity & Prevention o Passive and active immunization at the same time! o Give promptly to build antibodies to prevent virus attacking nervous system. o Vaccines include: human diploid cell vaccine, duck embryo vaccine, nerve tissue vaccine (brains of animals) inject into individuals. Arboviruses (Flavi, alphaviruses) Virus characteristics: o (+)ssRNA, lipid envelop (less stable), icosahedral o transferred by arthropods (West Nile virus) Disease characteristics:
o o
West Nile Virus (Flavivirus) spread by mosquitoes. Elder & immunocompromised more at risk for developing encephalitis. Asymptomatic Fevers, encephalitis (fatal, multiplies in non-neural tissue, found in blood,), hemorrhagic fever
Slow viruses Incubation periods are long & may appear many years later and are categorized conventional & unconventional. o Causes: spongiform o Symptoms include: loss of muscle control, shivering, tremors, & dementia o There is no inflammation, no immune response, no antigencity Prions: Infectious protein, no nucleic acid, cause degenerative neurological disease (scrapie) o 2 types of prions: PrPc: wildform, native, found on surface PrPsc: infectious form, tertiary structure o Replication: If PrPsc interacts with PrPc in the body will interact and change confirmation and infect near nerve cell & cause spongiform appearance. Conventional Slow Virus Disease - Subacute sclerosing panencephalitis (SSPE) measles virus Unconventional Slow Virus Diseases - Kuru: Neuro. disease in & children. Cannibalism. A prion - Creutzfeldt-Jakob: dementia, lesions resemble kuru - Scrapie: agent in brain. Sheep affected. spongiform encephal. - Transmissible mink encephalopathy: infects brain of mink - Bovine Encephalopathy (MAD COWS disease): spongiform
Hepatitis Viruses Definition: acute infections of the liver (jaundice) may lead to liver cancer (necrosis of hepatocytes) Viruses: herpes simplex, herpes-zoster virus, Epstein-Barr virus, coxsackieviruses o Viruses replicate primarily in the liver (viral hepatits): Hep A (HAV): infectious hepatitis w/ short incubation Hep B (HBV): serum hepatitis w/ long incubation due to blood/fluid exchange Hep C (HCV): non-A and non-B Hep D: super infection, more severe than other Hep, found mostly in pregnant women HAV: Picornovirus o (+)ssRNA, no envelop, enterovirus, spread by fecal-oral route (water, shellfish(raw clams)), infect liver, no cross react w/ Hep B o Disease: acute infection HBV: Hepadnavirus o dsDNA, enveloped, icosahedral, circular, variable in length. o Made up of 2 major proteins and 1 minor protein. o Can be seen as: Dane particle (complete virus), Sphere, or Filament with surface (s antigen) o Risk in drug abusers, transfusions, high promiscuous populations, infected blood, breast milk, saliva, nasopharyngeal, semen, menstrual fluid, blood. o Disease: acute & chronic infection o Replication: vRNA (pregenome RNA) copied into DNA by reverse transcriptase. Enzyme removes original vRNA and a double stranded DNA is formed. Virus is formed by budding. HCV: Flavivirus o (+)ssRNA, enveloped, icosahedral, lipid virus, related to plant virus, may cross a mammalian & plant virus o called non-A & non-B hepatitis o Disease: acute & chronic infection HDV: delta agent (viroid like) Fulminant hepatitis o ssRNA contains HBV surface protein. HDV is defective virus needs a helper fxn ex w/ HBV o super infection, intensify and becomes severe mostly in pregnant women
Oncogenes Virus RNA or DNA the cancer originates from a single cell Function of oncogene: protein kinases codes for tyrosine kinase that phosphorlyates proteins at tyrosine & causes fibrin network Human Leukemia-Sarcoma Virus: o Human Trophic cell leukemia virus HTLV-I and HTLV-II They are diploid cells, w/ 2 copies of genome, NOT segmented HTLV-1 via tax (transcriptional activation) activates IL-1, IL-2 receptor o HIV Binds to CD4 and chemokine receptor Treatment : AZT (azido-dideoxythymidine) Used for viral reverse transcriptase to prevent DNA replication, competes thymidine & terminates DNA growth. WBC Chain termination which does not allow anything to attach to the genome Anti-protease drugs: (ex. Saquinavir or Ritavir) Inhibit protease from cleaving the polyprotein into the virus. Protease cleaves the gag & pol to produce nucleocapsid proteins inhibits production of infection but does NOT cure infection. Replication:
o o o o o
Virus enters, cytoplasm is where the reverse transcriptase copies vRNA into complementary DNA DNA is called PROVIRUS & is found in linear & dsDNA form. DNA provirus gets into nucleus w/ pregenome chromosome, transcribes w/ infected virus mRNA translated into polyprotein (pp) ==> pp cleaved by proteus & assembled in plasma membrane virus buds from cell
Glycoprotein (glycosylated) gag = group specific antigen, capsid proteins pol = polymeras, protease, integrase env = enveloped glycoproteins LTR = aka long term repeats, these are promoters to enhance transcription factor binding sites
Misc: What replicates in the cytoplasm? pox virus cornovirus paramyxovirus rhabdovirus Guillan Baire Syndrome found in? EBV herpes Influenza (ortho) What is the difference between (+/-) sense? (-)sense means infected What type of vaccine do you need for rabies? both live & dead vaccine What are the 3 phases of Rhabdovirus? Prodromal ==> excitement ==> depression Which are associated with the common cold? coxsackieviruses rhinoviruses adenoviruses cornoviruses Which deals with cold sore? * Herpes labialis
Which viruses do you see coryza? Coronavirus paramyxovruses - Measles (Rubeola) which includes the 3Cs
What is the treatment for polio? aridone
Parasitology definition: reciprocal association, species depend upon another for its existence. Maybe temp. or permanent association: o symbiosis: o mutualism: o commensalisms: o parasite: weaker organism that obtains food & shelter from another & derives all benefits from association Types: ectoparasite: live outside of organism endoparasite: live inside of organism facultative: can have free form or w/in the organism obligate: completely establish only inside, cant live outside incidental: establish doesnt belong (its like an accident) temporary: part of life cycle in organism, later goes outside permanent: remains inside host pathogenic: causes injury, by trauma, toxins or damage pseudoparasite: like a parasite artifact coprozoic : termites able to digest cellulose (in the gut) Needs: Moisture & reasonable temperature Sources of infection: o Contamination, food, insects, animals, another person/fomite Hosts: o Definitive host: parasite reaches the sexual stage! o Intermediate host: o Paratenic host: it is a transfer host, of a parasite that is not essential to (neither hindering nor hastening) parasites life cycle o Incidental host: accidental o Dead-end host: o Reservoir host: Parasites can exist in 3 forms o Sporozite: resistant, quiescent (nothing happening) o Trophozoite: active eating stage o Larval forms:worms, cysts Lab diagnosis: Intestinal & biliary parasites o Feces (check 1st), intestinal material, Entero-Test method (get capsule w/ string parasite wrapped around when taken out) Common Human Infections o Protozaons o Nemathelminthes (round worms) o Platyhelminthes (flukes) o Arthropoda (fleas & ticks)
Protozoan Infections Disease name/agent Amebiasis Entameoba histolytica
Clinical condition intestinal diarrhea, dysentery
Infective form cyst, transmitted via food, water, anal intercourse
Diagnostic
Comments Can go into liver to cause abscesses
Treatment - metronidazole (M) + iodoquinol (intestinal) - (M) and dehydroemetine + chloroquine (extraintestinal) Topical miconazole for eye infection
Acanthamebiasis agent Acnthamoeba sp
- keratitis (eye) may lead to blindness - Chronic granulomatous amebic encephalitis
Giadrdiasis / Giardia lamblia Trichomoniassis Vaginal
protracted diarrhea and malabsorption syndrome vaginitis, itching, inflammation, discharge
- trophosoites, eye (contact lenses, soil, water sewage) found in brain tissue - maybe free living ameba cysts, persons to person contact, food, water (campers) trophozoite transmitted by veneral metratrypanosomes, transmitted by bite of TseTse fly
African Trypanosomiasis sleeping sickness, trypanosome brucei gambiense, trypanosome brucei rhodesiense American Trypanosomiasis / Trypanosoma cruzi
- skin lesion at bite site, fever, lymphadenopathy - CNS involvement: progressive mental, coma, death due to pneumonia - Starvation, sepsis - Chagas disease (in children) acute: visceral organs, heart, unilateral opthalmia, palpebral edema, eyes - Chronic disease (adults) : megaesophagus, megacolon, enlarged heart visceral leishmaniasis (kalaazar), destruction of macrophages, enlarged liver & spleen, protracted fever diarrhea & dysentery
stool, duodenal contents, cysts, trophozoites vaginal discharge, scrapings, trophozoite blood, CSF, lymph node aspirates, trypanosomes
animal reservoir (beavers, muskrats) pap smears, males (asymptomatic), no cyst form Winterbottoms sign (posterior cervical chain enlargement)
- quinacrine HCL, - metronidazole - furazolidine - metranidazole
- Gambian, - eflonithine, - Rhodesian, - Suramin, - Rhodesian encephalitis, - Melarsoprol B - Nifurtimox - benznidazole
trypomastigoes (body form) & transmitted by reduviid bug (kissing bug) feces
blood & trypomastigotes specific antibodies that bind to T. cruzi antigens bone marrow aspirate & macrophages
- xenodiagnosis: person suspected having acute disease - Host & resvoirs: domestic and wild animals - reservoir in dogs & foxes - thatched roofs, breeding places for sandflies largest protozoal parasite
Leishmaniasis
Promastigotes & Phlebotomus (sandfly)
- antimony compounds
Balantidiasis
- cysts, transmitted food & water contaminated by pigs
stool, cyst
- Iodoquinol
Plasmodiasis Malaria, plasmodium vivax, ovale, malariea, falciparium Toxoplasmosis Toxoplasma gondii
periodic fever, chills, hepatosplenomegaly, anemia - primary infection asymptomatic or mild - congenital infections (anomalies of CNS, eyes) - immunocompromised: disseminated infection involving CNS ingestion oocyts, meat containing tissue cysts
blood, cyclical plasmodial forms in RBC serum, tissues, organism not readily observed or cultured from humans
drug resistant in falciparum malaria
Chloroquine PO4, primaquine PO4, quinine for falciparum malaria pyramethamine + sulfadiazine
definitive host cat family
Babesiosis / Babesia microti
Nantucket fever, resembles malaria
bite of nymph of hard tick, Ixodes sacapularis
blood & organism in RBC
Cryptosporidiosis
profuse, watery diarrhea
oocysts, feces of animals, human feces & respiratory secretions
stool, gut tissue, oocyts observed via phase contrast microscopy, acid-fast stained material
important infection of domestic & wild animals & deer mice, field mice important reservoir Immunocompromised, fatal diarrhea, dehydration, parenteral nutrition, supportive
clindamycin + quinine
antibiotics not effective, immunocompetent self limiting, supportive care, paromomycin (some success)
Helminth Diseases (Round worms) Disease name/agent Clinical condition Ascariasis/ Most common in lumbricoides children, abdominal pain, obstruction or worm migration Hookworm / necator - Epigastric pain americanus or - anemia ancyclostoma duodenale Stronglyoidiasis / Watery, mucous diarrhea stercoralis Enterobiasis / E. vermicularis Trichinelliasis / larvae ingestion of meat Schistosomiasis / mansoni, haematobium Anal pruritus Muscle biopsy, serum,
Infective form Eggs, feces contaminated food or soil
Diagnostic Stool/ eggs
Comments
Treatment - Mebendazole - pyrantel pamoate
- larvae, (soil, on vegetative penetrate skin)
Stool /eggs
Controlled by sanitary disposal of human feces
- Mebendazole - pyrantel pamoate
Larvae / larvae in soil or vegetation penetrate skin Eggs / ingestion of eggs
Stool /eggs
anal contact spec/eggs curled up larvae in muscle, antibodies
ONLY nematode worm reproduce in host. Free living & parasitic phase Pinworm, seatworm infection Muscle worm infection
- Thiobendazole
- Mebendazole - pyrantel pamoate - steroids (severe) - Thiobendazole (adult)
* Taeniasis / saginata (beef) solium (pork)
* Diphyllobothriasis / latum * Tapeworm disease / Rat tapeworm / Hymenolepsis diminuta * Dwarf tapeworm / Hymenolepsis nana
Fever, lymph node & liver enlargement, obstruction of vessels of urinary bladder, intestine, liver Tapeworm infection, adult worm infect (asymptomatic) beef, epigastric fullness, nausea Fish tape worm, asymptomatic, diarrhea, anemia b/c lack of B12 Mild symptoms, loss of worm
Larvae (cercariae), larvae in snail infested water penetrate skin
Larvae (cysticercus), ingestion of raw/undercooked pork or beef Larvae (plerocercoid), ingestion of raw fish/undercooked fish Larvae, ingestion of infected cereals (flour)
Stool / eggs, worm segments Stool / eggs, worm segments Eggs in feces
T. solium may cause serious CNS infection (cysticercosis)
- prazquantel (unhooks)
- prazquantel (unhooks) - prazquantel (unhooks)
Abdominal pain, nausea & vomiting in heavy inf
Larvae, hand to mouth contact, ingestion of mouse feces
Eggs in feces
Most common tape worm in southeast US, children affected
- prazquantel (unhooks)
8/19/2006 Additional materials - Levines last lecture on parasitology - Enterococcus - M. Marium (Group I) - IMVIC (relevant lactose & gas), pg 33 - UPEC - Bortonella Quintana - Coxsacckie - Coronavirus - Orthomyxovirus - West Nile Virus (arbo virus) ==> What family does it belong to? Flavivirus - Oncogene
What is the difference between polio vs. poxvirus? Polio (+sRNA) Poxvirus (dsDNA) - Subgroup of the piconovirus - largest - vaccinated w/ Salk & Sabin - eradicated What is the difference btw the measles (rubeola) vs. German measles (rubella)? measles (rubeola) German measles (rubella) - acute infectious disease w/ rash & respiratory - subcategory of toga virus - 3C - (+)ssRNA, enveloped - no neuraminidase - rash on face - Kopliks spot - congenital anomalies - impairs CMI - SSPE - RSV: blocks resp. tract in young children

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Colony Cell Features Features

Source & Transmission

Virulence Factors (disease causing)

Host Defenses / Immunity

Gram (+) Cocci in cluster 1 u in diameter

Vancomycin (organism is resistant to most others)

Gram (+) Cocci in cluster 1 u in diameter

Source & Lab Characteristics Transmission

Host Defenses & Immunity

Lab Source & Characteristics Transmission

Host Defenses & Immunity

Cell Colony Features Features

Lab Source & Characteristics Transmission

Host Defenses & Immunity

Lab Source & Virulence Factors Characteristics Transmission

Host Defenses & Immunity

alpha hemolytic: partial breakdown of RBC,

Test Bile soluble Optochin

S. Pneumonoccus Cell lyses Cell lyses

Lab Source & Virulence Factors Characteristics Transmission

Host Defenses & Immunity

Normal & Damaged Acute Endocarditis - S. Aureus

Source & Virulence Factors Lab Characteristics Transmission

Host Defenses & Immunity

Source & Virulence Factors Lab Characteristics Transmission

Host Defenses & Immunity

Source & Virulence Factors Lab Characteristics Transmission

Host Defenses & Immunity

Source & Virulence Factors Transmission

Host Defenses & Immunity

Source & Virulence Factors Lab Characteristics Transmission

Host Defenses & Immunity

Source & Virulence Factors Transmission

Host Defenses & Immunity

Lab Characterist ics

Source & Transmission

Host Defenses & Immunity

Source & Transmission

Host Defenses & Immunity

Source & Transmission

Host Defenses & Immunity

Lipophilic diphtheroid (appeared in the test bank)

Source & Lab Characteristics Transmission

Host Defenses & Immunity

Source & Lab Characteristics Transmission

Host Defenses & Immunity

Nocardia brasiliensis major cause of actinomycetoma infections of foot

Lab Test Character.

Source & Transmission

Host Defenses Immunity

M. kansasii, M. marinum M. scrofulaceum M. avium-intracellulare complex M. fortuitum-chelonei complex Virulence Factors

Lab Source & Characteristics Transmission

Host Defenses & Immunity

Source & Lab Characteristics Transmission

Host Defenses & Immunity

Source & Lab Characteristics Transmission

Host Defenses & Immunity

Catalase (-) M. Bovis M. Leprae M. Avium Intracellulare (MAC) Acinetobacter

Catalase (+) M. Tuberculosis Norcadia

Source & Transmission

Host Defenses Immunity

Source & Transmission

Host Defenses Immunity

Source & Virulence Factors Lab Characteristics Transmission