Patho Test 2 Study Guide PDF

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Staphylococcus -

Characteristics -Gram positive cocci

- Causes wide range of infections

-Non-motile - Aerobic to facultative anaerobe

- Human colonizers: found on skin and mucous membranes

-Catalase positive

- S. aureus most virulent

-Tolerates high salt

- S. aureus only species that produces enzyme coagulase (coagulase positive)

-Grows at 18oC – 40oC

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Clinical Diseases of S. aureus S.aureus

Disease results from production of specific toxins

Coagulase Negative Staphlococci

Disease is caused by tissue destruction and proliferation of pathogen

- Endocarditis (native and prosthetic valves) -Catheter and Shunt infections -Prosthetic joint infections

Examples:

Examples:

-SSSS (Staphylococcal scalded skin syndrome)

-Cutaneous infections

-Urinary tract infections

-Bacteremia/Endocarditis

-Pneumonia/Empyema Staphylococci -Staphylococcal food - Osteomyelitis/Septic Arthritis Surface Protein A poisoning -capsule Teichoic Acid -Found on surface of S.aureus but NOT on -Toxic shock syndrome -peptidoglycan coagulase negative staph -Phosphate-containing polymers that are -teichoic acid covalently bound to the peptidoglycan - covalently linked to peptidoglycan -protein A layer. - mediate attachment to the mucosal surfaces through binding of fibronectin - species-specific. Polysaccharide A in S. aureus and polysaccharide B in S.epidermidis

-Protein A binds to Fc receptor of Capsule antibodies this providing protection from Peptidoglycan the humoral immune response -Slimy polysaccharide layer that lays over -one of the most important structures in cell surface - Extracellular form of protein A also binds staph antibodies, thereby forming immune - -Capsule produced during infection composed of layers of glycan chains complexes that consume the complement (repeating units of NAG and NAM) - Serotypes 5 & 8 associated with majority - Can be used to identify S aureus

 Pathogenesis and Immunity -Staphylococcal Toxins Alpha toxin Beta Toxin Gamma Toxin Exfoliative Toxin Enterotoxins Toxic Shock Syndrome Toxins Delta Toxin

Coagulase Alpha toxin -2 forms: free form and one bound to - Produced by most strains of S.aureus cell wall - Cytotoxin (toxin to many types of - Coagulase converts fibrinogen to host cells) fibrin which results in clumping of staphylococcal - Kills cells bycells integrating into membrane and forming pore. Leads to -The free form causes formation of leakage of ions, osmotic swelling, and clumps of fibrin in the blood cell lysis -Role of coagulase is believed to be Delta toxin avoidance of phagocytes by coating Beta Toxin the-Produced cells with fibrin by ALL S.aureus strains and -Heat labile protein produced by most most of coagulase negative strains strains Catalase - Cytotoxin (affects intracellular - cytotoxin membrane) - Produced by ALL staphylococci strains -Hydrolyses membrane phospholipids - Acts as a surfactant that disrupts which leads to lysis of cells

- Staphylococcal Enzymes Coagulase Catalase Hyaluronidase Fibrinolysin Lipases Nuclease Pennicillinase

Gamma Hemolysins Fibrinolysin of two polypeptide chains - aka-Composed staphylokinase (S and F) - Produced by ALL strains of S. aureus - Toxic to neutrophils and - Fibrinolysin dissolves fibrin clots macrophages which allows S. aureus to escape Cellclots lysis is mediated by pore blood formation Lipases -produced by ALL strains of S. aureus Exfoliative Toxin and more than 30% of coagulase- Produced by 5%-10% of S.aureus negative strains strains - hydrolyze lipids which allow - 2 forms: ETA and ETB staphylococci to utilize sebum for nutrition - ETA is heat stable and encoded by chromosome

Enterotoxins Hyaluronidase - 18 serologically enterotoxins -Produced by 90% of S.distinct aureus strains that are produced by 30%-50% of - Degrades hyaluronic S.aureus strains acids which form the cellular matrix of the host tissue- Cause staphylococcal food poisoning Cause Toxin shock syndrome - This -enzyme allows S. aureus to when actone as superantigens spreadthey from tissue to the other - Staphylococcal food poisoning (SFP) is abrupt and rapid in response to Nuclease toxins and characterized by severe -S. aureus produces a nuclease which vomiting, diarrhea, and abdominal degrades pain.nucleic acids - Role-Treat of nuclease in pathogenesis is and with replacement of fluids not known relief from pain - Nuclease probably allows S. aureus l i id f ii

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hy i staph on their s co n, the nasophar d ur Shedding of s responsible for nosocomial infections Staph’s ability to survive in dry environments also contributes to the prevalence of infections by these organisms

Laboratory Diagnosis

Can be identified with several techniques: -

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Microscope with gram stain Culture with high salt Serology is used to identify staph in bacterimic patients Biochemical tests Antibiotic susceptibility may be necessary if antibiotic resistance is suspected Culture: S.aures = golden / Coagulase negative is white

Treatment and Prevention - Treatment: Less than 10% susceptible to penicillin, semisynthetic penicillin, Vancomycin when resisitance to methicillin - Prevention: Staph are ubiquitous and best prevention is proper cleansing of skin cuts and wounds

Streptococcus Characteristics -

Gram positive cocci Facultative anerobes Chains

Grown on agar enriched with blood Classification  Hemolytic activity on blood agar - Complete(beta) - Incomplete(alpha) - None(lambda) Streptococcus pyogenes (Group A) -

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Characteristics - -Inhibited by high concentration of sugar - -colonies show large zone of beta hemolysis - -encapsulated strains appear mucoid on freshly prepared media but wrinkled in dry - -non-encapsulated strains are smaller and glossy Clinical Diseases of S. Pyogenes (group A)

Suppurative S. pyogenes dieases (pus forming) -

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Pharyngitis: strep throat; fever, chills, malaise, headache. Pus pockets seen on back pharynx Scarley fever: complication of pharyngitis;toxin produced causes body

Nonsuppurative S. pyogenes disease -

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Rheumatic fever: inflammation that involves heart, joints, blood vessles. Occurs in pts with sever pharyngitis Acute glomerulonephritis: inflammation of kidneys

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Surface Components of S. pyogenes (group A) Other Surface components

Type Specific Proteins-Surface proteins are also used to differentiate between S. pyogenes strains -

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M Protein: adhesin that mediates invasion of epithelial cells; degrades complement components C3b(antiphagocytic) T Protein: used to differentiate strains when M protein is not expressed. T is involed In adhesion and invasion

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M-like proteins Lipoteichoic acid:medicate host cell binding by fibronectin F Protien: mediate binding by fibonectin

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Composed of hyaluronic acid Provides protection form phagocytosis

Group A specific carbohydrate: -

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Group A is different from other strep by specific antigen on cell wall A possess a carbohydrate that is a dimer of Nacetylglucosamine and rhamnose

Pathogenesis and Immunity - Adhesion of host cells - Invasion of host cells - Avoidance of host defenses - Production of toxins

Adhesion of host cells -

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Capsule- Slimy outer most layer of cell

Mediated by: lipoteichoic acid, M protein, and F proteins I ii l d k

Invasion of Host cells -

Mediated by: M and F Responsible for recurrent infection I i f i h li l

Avoidance of host defenses -

Mediated by M protein M binds ot regulatory protein of the alternative complement pathway(factor H), hi h d d C3b li i

Production of Toxins: Deoxyribonucleases -

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Four (A,B,C,D) Depolymerize free DNA in pus to redeuce viscosity in skin abcess This allows pathogen to the upper respiratiory tract and skin of healthy people spread to other tissue n dry surfaces for long periods of time

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Spreads by respiratory droplets or breaks of skin Children are most susceptible to pharyngitis

 Laboratory Diagnosis - Mircorsopy: Gram positive cocci in pairs and chains - Presence of strep on specimens form upper respiratory tract is NOT sign of disease - Antigen Dection: antibodies that react wit the group of specific carbohydrate - Culture: Throa swabs have to be taken from posterior oropharynx . Identified by direct antigen detection of group specific carbohydrate  Treatment, Prevention, and Control - S. pyogenes is sensitive to penicillin - Ocacillin or vancomycin is sued in the case that S. pyogenes is mixed with S. aureus - Drainage and debridement is necessary in soft tissue infections Streptococcus pneumoniae  Characteristics - Encapsulated gram positive coccus - Large colonies - Round and mucoid colonies

- Alpha hemolytic when grown aerobically but beta when grown anaerobically - Grown on media supplemented with blood  Clinical Diseases Pneumonia: inflammation of the lungs; caused by growth of S. pneumoniae in the alveolar spaces; alveoli become blocked with pus and cause solidification of lung; coughing, shortness of breath, chest pain

Meningitis: occus when pathogen spreads to central nervous system after bacteremia or other infections

Sinusitis and otitis media: infection of paranasal sinuses and ear. Preceded by viral infection Bacteremia: pathogen in blood stream. Could be due to d immunity of S. pneumoniae complications of pneumonia or meningitis. Can lead to endocarditis esponse and not by secreted toxins

Phagocytic Survival

Tissue Destruction

- Survives phagocytosis because of capsule

Teichoic acid and peptidoglycan fragments of S. pneumoniae activate the alternative complement system(c5a) This leads to inflammation

-Pneumolysin is cytotoxic to phagocytes -Uses phosphatidycholine to bind receptors or platelet activating factor. These receptors allow the pathogen to enter host tissue cells and be protecting from complement sys and phagocytosis Colonization and Mirgration -Colonizes the oropharynx and spreads to the lungs, paranasal sinuses, or middle ear -Surface protein adhesions are used ot bind epithelial cells. -Evades the action of IgA by producing the IgA protease -Produces a cytoxin that destroys chiliated spithelial cells

-This activation is stimulated by the autolysin which releases cell wall components -Pneumolysin activates the classic pathway of the complement sstem C5a and C3a leading to inflammation -Cytokines are produced bby activiated leukocytes which leads to more inflammation -All this results in fever and tissue damage

Epidemiology More common in cool months Colonization is high in young children Infections are caused by endogenous spreading from colonized throat Droplet transmission is rare Laboratory Diagnosis Microscopy: gram stain of sputum reveals lancet shape gram positive diplococci. Usually surrounded by unstained capsule - Identification: autolysis is active by bile. Addition of bile on a colony results in solubility of the colony in a few minutes. - S. pneumoniae is also susceptible to optochin - Culture: culture of sputum does not always yield growth because of contaiminating oral flora  Treatment, Prevention, and Control - Pencilllin is effective - Cephalosporin, erythromycin and chloramphenicol are sued in case of resistance or allergy to penicillin   -

Bacillus

Bacillus anthracis 

Characteristics - Most important pathogen in genus bc serious infections that it causes AND its use as a biological weapon.

 Physiology and Structure - Gram-positive rods in pairs or chains. Form clumps in culture - Large cells - Spores form after 2-3 days in culture but not spores in specimens

 Clinical Diseases Inhalation (pulmonary) Anthrax Cutaneous Anthrax - most common form of anthrax - Affects skin after inoculation of site of injury by B. anthracis. - Characterized by: development of painless papule at injury site. Papule progresses rapidly into an ulcer which results in necrosis of affected tissue -Mortality rate: 20%

(1)Capsule, (2)exotoxins, (3)endospores

Gastrointestinal Anthrax - Affect upper intestinal tract, where mouth or esophagus shows ulcers. Leads to edema and sepsis.

- Occurs when spores of B. anthracis are inhaled  into the lungs

Pathogenesis - Condition may remain asymptomatic for likeImmunity 2 or more months where spores and remain Utilizes: in the lymph nodes

- Affects lower intestinal tract where symptoms are nausea, vomiting and - Manifestation of the disease begins with Protective antigen: antigen malaise. Condition can progress to Exotoxins fever, shortness of breath, Capsule responsible for binding to host cough, systemic disease rapidly headache, vomiting, chills, and chest, and cell of amino acids - 3 exotoxins produced - Composed abdominal pains - Mortality rate: close to 100% factor: adenylate cyclase. 1. Protective antigen - 3 genesEdema responsible (capA, capB, by antibiotics at - If disease not stopped Factor increases the [cAMP] in capC) for capsule synthesis this point, then the B. anthracis enters the 2. Edema factor host cell which is responsible for blood stream proliferate, leading to - Capsulefluid genes carried on and plasmid accumulation observed 3. Lethal factor septic shock. Kills patient in 24-36 hours - CapsuleLethal allowsfactor: B. anthracis zinc to avoid -Genes encoding toxins on Mortality rate: close to 100% phagocytosis metalloprotease that causes plasmid stimulation of cytokine release - These 3 factors combine to form and host cell death by cleaving two effective toxins: edema toxin several kinases which leads to and lethal toxin apoptosis

Edema toxin = combo of protective antigen and lethal factor Lethal toxin = combo of protective and lethal factor

***2 toxins plus capsule responsible for disease

Capsule Endospore

Endospore formation: - Type of resting cell highly resistant to heat, radiation, and disinfectants - Forms endospores in response to starvation. Stays like this till better conditions - Endospore formation main characteristic that leads to its use as biological weapon

1. Spore formation begins to isolate newly replicated DNA and a small portion of cytoplasm 2. Plasma membrane starts to surround DNA, cytoplasm, and membrane isolated in strep

3. Spore septum surrounds isolated portion, forming forespore. 4. Peptidoglycan layer forms between membranes 5. Spore coat forms 6. Endospore is freed from cell

 Epidemiology - Affects herbivores (cattle and sheep) primarily and humans accidental host - Anthrax infections rare in developed countries but common in poorer countries - People at risk are those who work close with animals or animal products - Cutaneous anthrax 95% of cases - Gastrointestinal anthrax is rare in humans but more common in herbivores - Inhalation anthrax rare but scary bc this is mode used as biological weapon - NO person to person transmission

 Laboratory Diagnosis - Microscope and culture - Microscope shows gram-positive bacilli - Spores not observed in microscope evaluation bc only form if starving - Grow on most nonselective media - Colonies are nonhemolytic and very sticky on agar

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Biochemical tests and serology can be used for definitive identification

Treatment, Prevention, and Control - Control: Control in humans requires control in animal by vaccination and by culling/destruction of infected animals - Burning and burying of animals that die of anthrax is important - Vaccination is limited to individuals who work closely with animals

Bacillus cereus -

Opportunistic pathogen

 Clinical diseases Gastroenteritis (emetic form)

Gastroenteritis (diarrheal form)

- Results from consumption of contaminated rice.

- Results from consumption of contaminated meat and veggies.

- Spores allow B. cereus to k f

- Organism multiplies in the l d d

Ocular infection/ catheter infections/endocarditis - Ocular infections results in complete loss of sight after inoculation of an eye injury with

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1.) Heat stable enterotoxin that causes emetic form of gastroenteritis.

Mechanism of toxin is unknown

2.) Heat-labile enterotoxin that causes diarrheal form of gastroenteritis.

Mechanism: stimulates adenylate cyclase which increases the level of cAMP in host cells and cause diarrhea

 Epidemiology - Ubiquitous in the environment  Laboratory Diagnosis - Grows well on nonselective media - Culture from contaminated food can be used to determine presence of B. cereus - Isolation from patient is of no value bc fecal contamination is common - With ocular/catheter infections: gram stain used to detect  Treatment, Prevention, and Control - Treatment: Course is so short, antibiotics not necessary - Prevention: Food poisoning may be prevented by immediately consuming or refrigerating food after cooking - Treatment of other infections complicated because of the rapid course of infection and the high incidence of penicillin and cephalosporin resistance - Vancomycin, clindamycin, ciprofloxacin, and gentamicin may be used to treat ocular or catheter infections - Proper cleaning of wounds prevents infections  Anthrax as a biological weapon - B.anthracis spores are (1)easy to produce, (2)last a long time, and (3)anthrax has a high mortality rate - These characteristics are why anthrax is used as biological weapon

Listeria 1. Characteristics - Gram-positive cocci - Facultative anaerobes - Short: can be single, in pairs, or in chains - Sometimes mistaken for strep or enterococci - Cold tolerant 2. Clinical Diseases - Neonatal Disease - Listeriosis - Primary bacteremia Neonatal Disease Acquired during/after birth

Acquired in utero -Early onset bacteremia

Listeriosis -Can be asymptomatic in healthy adults - Sometimes flu-like or gastrointestinal symptoms

-Late onset meningitis (develops 2-3 weeks after birth)

-Severe in patients with compromised immunity

1. 2. 3. 4. 5. 6. 7. 8.

Primary Bacteremia - When L. monocytogenes invades blood stream

Pathogenesis and - low mortality rates (except Immunity immunocompromised) Enters epithelial cells ofcan be mild - Symptoms chills/fever intestine, then to severe fever enters blood

stream - Infected host cells eventually die by apoptosis or necrosis Intracellular life cycle of listeria: Entry into host cell by induced phagocytosis using internalins (proteins that interact with surface proteins of host) Transient(short) residence within a phagocytic vacuole Escape from vacuole to the cytoplasm using exotoxins, enzymes, and listeriolysin O that disrupts the phagosome membrane Cytosolic replication and recruitment of host cell actin onto bacterial surface Actin-based motility by formation pf pseudopods. Motility mediated by protein ActA, which mediates assembly of actin Phagocytosis of pseudopods by neighboring cells Formation of a double membrane phagosome Escape from secondary phagosome

9. Re-initiation of cell-cycle *humoral immunity is not effective because its intracellular 4. Epidemiology - Found in many environmental sources (soil, water, food, feces) - Fecal-oral enrichment cycle - Infections occur in compromised individuals (immunocompromised, ...