front 1 GRAM POSITVE BACTERIA | back 1 STAIN PURPLE WHEN GRAM STAINED FALL INTO PHYLUM FIRMICUTES TWO MAJOR GROUPS: LOW G+C GRAM POSITIVE AND HIGH G+C GRAM POSITIVE |
front 2 STAPHYLOCOCCUS (GENUS) | back 2 ARE LIVING AND REPRODUCING ON ALMOST EVERY SQUARE INCH OF YOUR SKIN. CAN BE OPPORTUNISTIC PATHOGENS NORMAL MEMBERS OF HUMANS MICROBIOTA S. AUREUS AND S. EPIDERMIDIS |
front 3 STAPHYLOCOCCUS | back 3 GRAM POSITIVE FACULTATIVE ANAEROBES; PROKARYOTIC SPHERICAL CELLS ARE CLUSTERED IN GRAPELIKE ARRANGEMENTS CAPABLE IN GROWING IN MEDIA THAT ARE 10% NACL (SALT) SYNTHESIZES CATALASE |
front 4 S. AUREUS S. EPIDERMIDIS | back 4 S. AUREUS: MORE VIRULENT, PRODUCES A VARIETY OF DISEASE CONDITIONS AND SYMPTOMS DEPENDING ON SITE OF INFECTION. S. EPIDERMIDIS: NORMAL MICROBIOTA ON HUMAN SKIN. OPPORTUNISTIC PATHOGEN IN IMMUNOCOMPROMISED PATIENTS, OR WHEN INTRODUCED BY CATHETERS OR PROSTHETIC DEVICES. |
front 5 STAPHYLOCOCCUS PATHOGENICITY | back 5 CAUSED WHEN STAPHYLOCOCCI BREACH BODY'S PHYSICAL BARRIERS (SKIN OR MUCUS MEMBRANES) RESULTS FROM THREE FEATURES: -STRUCTURES THAT ENABLE IT TO EVADE PHAGOCYTOSIS -PRODUCTION OF ENZYMES -PRODUCTION OF TOXINS |
front 6 STRUCTURAL DEFENSES (STAPHYLOCOCCUS) PROTEIN A | back 6 THE CELLS OF S. AUREUS ARE UNIFORMLY COATED WITH PROTEIN = PROTEIN A -INTERFERES WITH ANTIBODY IMMUNE RESPONSES BY BINDING TO CLASS G (IGG) ANTIBODIES. ANTIBODIES--> OPSONINS INHIBIT OPSONIZATION INHIBITS COMPLEMENT CASCADE |
front 7 STRUCTURAL DEFENSES STAPHYLOCOCCUS BOUND COAGULASE | back 7 ENZYME THAT CONVERTS FIBRINOGEN INTO LONG INSOLUBLE FIBRIN MOLECULES. HIDES BACTERIA IN CLOTS FROM PHAGOCYTES S. AUREUS AND S. EPIDERMIDIS: EVADE BODY DEFENSES BY SYNTHESIZING LOOSELY ORGANIZED POLYSACCHARIDE SLIME LAYERS OR CAPSULES INHIBITS CHEMOTAXIS OF AND ENDOCYTOSIS BY LEUKOCYTES NEUTROPHILS FACILITATES ATTACHMENT TO ARTIFICIAL SURFACES (E.G. CATHETERS, SHUNTS, ARTIFICIAL HEART VALVES) |
front 8 ENZYMES STAPHYLOCOCCUS (CELL FREE COAGULASE; HYALURONIDASE) | back 8 C.F. COAGULASE: TRIGGERS BLOOD CLOTTING; COMBINES WITH BLOOD PROTEIN BEFORE BECOING ENZYMATIC AND CONVERTING FIBRINOGEN TO FIBRIN THREADS ONLY S. AUREUS SYNTHESIZES COAGULASE H.: BREAKS DOWN HYALURONIC ACID; WHICH IS MAJOR COMPONENT OF MATRIX BETWEEN CELLS. FOUND IN 90% OF S. AUREUS STRAINS, ENABLES BACTERIA TO SPREAD BETWEEN CELLS THROUGHOUT THE BODY. |
front 9 ENZYMES S. AUREUS STAPHYLOKINASE, LIPASES (S. AUREUS, S. EPIDERMIDIS) | back 9 STAPHYLOKINASE: DISSOLVES BLOOD CLOTS IN FIBRIN THREADS IN BLOOD CLOTSALLLOWING S. AUREUS TO FREE ITSELF FROM CLOTS. CAN ESCAPE IMMUNE SYSTEM BY ENCLOSING ITSELF IN FIBRIN CLOT (COAGULASE) CAN DIGEST ITSELF OUT OF CLOT WITH STAPHYLOKINASE AND SPREAD TO NEW LOCATIONS. LIPASES: DIGEST LIPIDS, ALLOWING STAPHYLOCOCCI TO GROW ON THE SURFACE OF THE SKIN AND CUTANEOUS OIL GLANDS. ALL STAPH PRODUCE LIPASES. |
front 10 ENZYMES S. AUREUS BETA-LACTAMASE | back 10 AKA PENICILLINASE: NOW PRESENT ON 90% OF S. AUREAUS STRAINS; BREAKS DOWN PENICILLIN. ALLOWS BACTERIA TO SURVIVE TREAMENT WITH BETA-LACTAM ANTIMICROBIAL DRUGS SUCH AS PENICILLIN AND CEPHALOSPORIN |
front 11 TOXINS CYTOLYTIC TOXINS | back 11 ALPHA, BETA, GAMMA AND DELTA TOXINS ARE PROTEINS CODED BY CHROMOSOMAL GENES THAT DISRUPT CYTOLASMIC MEMBRANES OF A VARIETY OF CELLS, INCLUDING LEUKOCYTES (WBCS) LEUKOCIDIN- A 5TH CYTOLYTIC TOXIN; LYSES LEUKOCYTES PROVIDES STAPHYLOCOCCUS PROTECTION AGAINST PHAGOCYTOSIS |
front 12 TOXINS EXFOLIATIVE TOXINS | back 12 EACH OF TWO DISITNCT PROTEINS CAUSES THE DISSOLUTION OF EPIDERMAL DESMOSOMES CAUSING PATIENTS SKINS CELLS TO SEPARATE FROM EACH OTHERAND SLOUGH OFF OF BODY. |
front 13 TOXIC SHOCK SYNDROME (TSS) TOXIN | back 13 THIS PROTEIN CAUSES TSS WHEN STAPHYLOCOCCUS PRODUCING TSS TOXIN GROW IN A WOUND OR ABRAIDED VAGINA, TOXIN CAN BE ABSORBED IN THE BLOOD AND CAUSE TSS, NON-STREPTOCOCCAL TSS. S. AUREUS GROWS WELL IN SUPER ABSORBENT TAMPONS THAT STAY IN PLACE FOR LONG PERIODS OF TIME. |
front 14 ENTEROTOXINS | back 14 5 PROTEINS DESIGNATED (A THROUGH E) STIMULATE THE INTESTINAL MUSCLE CONTRACTIONS; NAUSEA AND INTENSE VOMITING ASSOCIATED WITH STAPHYLOCOCCAL FOOD POISONING ARE HEAT STABLE; REMAINING ACTIVE AT 100 C FOR UP TO 30 MINUTES |
front 15 EPIDEMIOLOGY S. AUREUS, S. EPIDERMIDIS | back 15 S.E: IS UBIQUITOUS ON HUMAN SKIN S.A.: FOUND ONLY ON MOIST SKIN FOLDS BOTH GROW IN UPPER RESPIRATORY, GASTROINTESTINAL AND UROGENITAL TRACTS BOTH CONTRACTED BY FOMITES AND DIRECT CONTACT PROPER HAND WASHING AND ASEPTIC TECHNIQUES ARE ESSENTIAL TO PREVENTION N HEALTHCARE SETTINGS |
front 16 NONINVASIVE DISEASE | back 16 S. AUREUS: ONE OF MORE COMMON CAUSES OF FOOD POISONING; FOOD INTOXICATION; ENTEROTOXIN CONTAMINATED FOOD COMMONLY AFFECTED FOOD: PROCESSED MEATS, CUSTARD PASTRIES, POTATO SALAD, AND ICE CREAM WARMING OR REHEATING DOESN'T INACTIVATE ENTEROTOXIN, WHICH ARE HEAT STABLE ; HEATING DOES KILL THE BACTERIA COURSE OF DISEASE IS 24 HRS OR LESS |
front 17 CUTANEOUS DISEASES STAPHYLOCOCCAL SCALDED SKIN SYNDROME IMPETIGO | back 17 S. AUREUS CAUSES LOCALIZED PYOGENIC LESIONS S.S.SKIN SYNDROME: REDDENING OF SKIN, BEGINS AT THE MOUTH SPREADS OVER ENTIRE BODY; FOLLOWED BY LARGE BLISTERS (BLISTERS HAVE NO BACTERIA OR WBC) IMPETIGO: SMALL, FLATTENED, RED PATCHES ON FACE, AND LIMBS PARTICULARLY ON CHILDREN WHOSE IMMUNE SYSTEMS ARENT DEVELOPED. |
front 18 CUTANEOUS DISEASES FOLLICULITIS STY FURUNCLE/ CARBUNCLE | back 18 FOL.: INFECTION OF THE HAIR FOLLICLE, BASE OF FOLLICLE BECOMES SWOLLEN AND PUS FILLED. AT BASE OF EYELID ITS CALLED A STY FUR.: BOIL, IS LARGE PAINFUL NODULAR EXTENSION OF FOLLICULITIS INTO SURROUNDING TISSUE. CARB.: WHENN SEVERAL FURUNCLES COALESCE. EXTENDS DEEPER INTO TISSUES, TRIGGERING FEVER AND CHILLS; CHARACTERISTIC OF INNATE IMMUNITY |
front 19 BACTEREMIA | back 19 S. AUREUS COMMON CAUSE OF BACTERIA IN THE BLOOD. FURUNCLES, VAGINAL INFECTIONS, AND CONTAMINATED MEDICAL DEVICES HAVE ALL BEEN IMPLICATED IN CASES. NOSOCOMIAL INFECTIONS ACCOUNT FOR HALF OF ALL CASES. |
front 20 ENDOCARDITIS | back 20 S. AUREUS MAY ATTACK THE LINING OF THE HEART INCLUDING THE VALVES. PATIENTS HAVE NON SPECIFIC FLU LIKE SYMPTOMS BUT QUICKLY DETERIORATE; AMOUNT OF BLOOD PUMPED FROM HEART DROPS. 50% DO NOT SURVIVE |
front 21 PNEUMONIA AND EMPYEMA | back 21 STAPHYLOCOCCUS IN THE BLOOD CAN INVADE THE LUNGS; CAUSING PNEUMONIA INFLAMMATION OF LUNGS WHEN AVEOLI AND BRONCHIOLES BECOME FILLED WITH FLUID. IN 10% OF PATIENTS WITH STAPHYLOCOCCAL PNEUMONIA (FLUID IS PUS) CONDITION KNOWN AS EMPYEMA. |
front 22 OSTEOMYELITIS | back 22 WHEN STAPHYLOCOCCUS INVADES A BONE VIA TRAUMATIC WOUND OR VIA BLOOD DURING BACTEREMIA. INFLAMMATION OF BONE MARROW AND SURROUNDING BONE. CHARACTERIZED BY PAIN IN BONE AND HIGH FEVER. IN CHILDREN OCCURES IN GROWING LONG BONES. ADULTS IN VERTEBRAE. |
front 23 DIAGNOSIS OF STAPHYLOCOCCUS | back 23 IF STAPHYLOCOCCI ISOLATED FROM AN INFECTION ARE ABLE TO CLOT BLOOD, THEN THEY ARE COAGULASE POSITIVE S. AUREUS. GRAPELIKE ARRANGEMENTS COAGULASE NEGATIVE STAPHYLOCOCCI ARE USUALLY S. EPIDERMIDIS 90% OF STAPHYLOCOCCI WERE SUSCEPTIBLE TO PENICILLIN IN 1945; ONLY 5% TODAY |
front 24 MRSA/ VRSA | back 24 METHICILLIN RESISTANT STAPHYLOCOCCUS AUREUS MORE POEPLE DIE OF MRSA THAN HIV IN U.S. MRSA IS RESISTANT TO: PENICILLIN, MACROLIDES, AMINOGLYCOSIDES, AND CEPHALOSPORIN VANCOMYSIN IS USED TO TREAT MRSA CURRENTLY THERE IS NOW SOME VANCOMYSIN RESISTANT STAPHYLOCOCCUS AUREUS - VRSA |
front 25 STAPH PREVENTION | back 25 PROPER CLEANSING OF WOUNDS AND SURGICAL OPENINGS ASEPTIC USE OF CATHETERS AND INDWELLING NEEDLES APPROPRIATE USE OF ANTISEPTICS HANDWASHING |
front 26 STREPTOCOCCUS | back 26 GRAM POSITIVE; ARRANGED IN PAIRS (DIPLO) OR CHAINS COCCUS; COCCI (SPHERICAL SHAPED) CATALASE NEGATIVE SYNTHESIZES PEROXIDASE; FACULTATIVELY ANAEROBIC DIFFERENTIATE SPECIES USING SEROLOGICAL CLASSIFICATION (CREATED BY REBECCA LANCEFIELD 1895-1981) |
front 27 LANCEFIELD GROUPS | back 27 SEROTYPE GROUPS (LANCEFIELD GROUPS) A TO H, AND K TO V A, AND B MORE SIGNIFICANT STREPTOCOCCAL PATHOGENS IN HUMANS TWO OTHERS LACK LANCEFIELD ANTIGENS |
front 28 GROUP A STREPTOCOCCUS | back 28 S. PYOGENES- FORMS WHITE COLONIES 1-2MM IN DIAMETER SURROUNDED BY LARGE ZONE OF BETA-HEMOLYSIS AFTER 24 HRS ON BLOOD AGAR PATHOGENIC STRAINS FORM CAPSULES |
front 29 GROUP A STREPTOCOCCUS PATHOGENICITY (M PROTEIN, HYALURONICACID CAPSULE ) | back 29 M.P.: MEMBRANE PROTEIN DESTABILIZES COMPLEMENT. INTERFERES WITH OPSONIZATION AND LYSIS. H.A.C.: H.A. FOUND IN BODY; WBC MAY IGNORE CAMOUFLAGED BACTERIA WITH THIS TYPE OF CAPSULE. |
front 30 GROUP A STREPTOCOCCUS PATHOGENICITY | back 30 2 STREPTOKINASES - BREAKS DOWN CLOTS 4 DEOXYRIBONUCLEASES - DEPOLYMERIZES DNA C5a PEPTIDASE - BREAKS DOWN COMPLEMENT OF C5a PROTEIN S. PYOGENES DECREASES MOVEMENT OF WBCS TO INFECTION SITE |
front 31 GROUP A SREPTOCOCCUS PATHOGENICITY TOXINS | back 31 SECRETES 3 DISTINCT TOXINS - PYROGENIC TOXINS -STIMULATE MACROPHAGES AND HELPER T LYMPHOCYTES TO RELEASE CYTOKINES - STIMULATE FEVER, RASH, SHOCK -AKA ERYTHROGENIC TOXINS TOXINS CARRIED ON TEMPERATE BACTERIOPHAGES- ONLY LYSOGENIZED BACTERIA SECRETE TOXINS |
front 32 GROUP A PATHOGENICITY | back 32 S, PYOGENES PRODUCES TWO TYPES OF MEMEBRANE BOUND PROTEINS CALLED STREPTOLYSINS LYSE RBCS, WBCS, AND PLATELETS INTERFERE WITH OXYGEN CAPACITY OF BLOOD, IMMUNITY AND BLOOD CLOTTING |
front 33 GROUP A EPIDEMIOLOGY | back 33 FREQUENTLY INFECTS PHARNYX OR THE SKIN CAUSES DISEASE ONLY WHEN NORMAL COMPETEING MICROBIOTA ARE DEPLETED CAN AFFECT DEEP TISSUE WITH BREAK IN BARRIERS OF SKIN IS SPREAD BY RESPIRATORY DROPLETS |
front 34 GROUP A STREPTOCOCCAL DISEASES PHARYNGITIS, SCARLET FEVER | back 34 P: SORE THROAT CAUSED BY STREPTOCOCCI, COMMONLY KNOWN AS STREP THROAT, IS A KIND OF PHARYNGITIS; ITS INFLAMMATION OF THE PHARNYX, ACCOMPANIED BY FEVER, MALAISE AND HEADACHE. BACK OF PHARNYX RED WITH SWOLLEN LYMPH NODES AND PURULET ABSCESSES COVERING TONSILS. S.F.: "SCARLETINA" OFTEN ACCOMPANIES STREPTOCOCCAL PHARYNGITIS WHEN THE INFECTION INVOLVES A LYSOGENIZED STRAIN OF s. PYOGENES. RASH ON BODY AND STRAWBERRY COLORED TONGUE. RASH DISAPPEARS IN A WEEK AND FOLLOWED BY SLOUGHING SKIN. |
front 35 GROUP A STREPTOCOCCAL DISEASES PYODERMA AND ERYSIPELAS STREPTOCOCCAL TSS | back 35 P AND E: PYODERMA IS A CONFINED PUS PRODUCING LESION THAT USUALLY OCCURS ONTHE EXPOSED SKIN OF THE FACE ARMS OR LEGS. CAN BE CONTRACTED BY DIRECT CONTACT WITH INFECTED PERSON OR FOMITES. AKA IMPETIGO (STREP. VERSION) WHEN STREPTOCOCCAL INFECTION INVOLVES SURROUNDING LYMPH NODES AND TRIGGER PAIN AND INFLAMMATION ITS CALLED A ERYSIPELAS. MOST COMMON ON CHILDRENS FACES. S.TSS: CAN SPREAD AND LEAD TO BACTEREMIA AND SEVERE MULTI SYSTEM INFECTIONS PRODUCING STSS. CAUSES INFLAMMATION AT SITE OF INFECTION, PAIN, FEVER, CHILLS, MALAISE NAUSEA VOMITING, AND DIARRHEA. FOLLOWED BY INCREASED PAIN, ORGAN FAILURE, SHOCK. 40% PATIENTS DIE. |
front 36 GROUP A STREPTOCOCCAL DISEASES NECROTIZING FASCIITIS RHEUMATIC FEVER | back 36 N.F: "FLESH EATING BACTERIA", STREPTOCOCCI ENTER THE BODY THROUGH BREAKS OF SKIN, SECRETE TOXINS AND ENZYMES THAT DESTROY TISSUE, AND EVENTUALLY MUSCLE AND FAT TISSUE ARE DESTROYED. SPREAD DEEP IN TISSUE ALONG THE FASCIA. ALSO INVOLVES TOXEMIA (TOXINS IN BLOOD). FAILURE OF MAN ORGAMS. 50% PATIENTS DIE. R.F: COMPLICATION OF UNTREATED S. PYOGENES PHARYNGITIS. INFLAMMATION LEADS TO DAMAGE OF HEART VALVES AND MUSCLE. ITS AN AUTOIMMUNE RESPONSE; SREPTOCOCCAL ANTIGENS CROSS REACT WITH HEART ANTIGENS. MORE PREVELANT BEFORE ANTIMICROBIAL DRUGS. |
front 37 GROUP A STREPTOCCCAL DISEASES GLOMERULONEPHRITIS | back 37 G.: STREPTOCOCCUS GROUP A ARE NOT REMOVED FROM CIRCULATION BUT INSTEAD ACCUMULATE IN THE GLOMERULI (SM. BLOOD VESSELS) OF THE KIDNEYS NEPHRONS (FILTERING UNITS). RESULT IS GLOMERULONEPHRITIS. INFLAMMATION OF THE GLOMERULI AND THE NEPHRONS LEADING TO HYPERTENSION. AND LOW URINE OUTPUT. |
front 38 GROUP B STREPTOCOCCUS S, AGALACTIAE | back 38 GRAM POSITIVE COCCUS, .6-1.2 UM D. DIVIDESTO FORM CHAINS, BETA HEMOLYTIC. HAS: GROUP SPECIFIC POLYSACCHARIDE CELL WALL ANTIGENS, FORMS BUTTERY COLONIES 2-3 MM IN D, SMALL ZONE OF BETA HEMOLYSIS AFTER 24 HRS OFGROWTH ON BLOOD AGAR, BACITRACIN RESISTANT. |
front 39 GROUP B STREPTOCOCCUS PATHOGENICITY | back 39 S. AGALACTIAE DO FORM CAPSULES, ANTIBODIES TARGET ITS CAPSULAR ANTIGENS, SO CAPSULES ARE NOT PROTECTIVE. HAS A PREDI;ECTION FOR NEWBORNS WHOVE NOT YET FORMED TYPE SPECIFIC ANTBODIES. PRODUCE ENZYMES- PROTEASES (CATABOLZE PROTEINS) , HEMOLYSINS (LYSE RED BLOOD CELLS) DEOXYRIBONUCLEASE , HYALURONIDASE |
front 40 GROUP B STREPTOCOCCUS EPIDEMIOLOGY | back 40 NORMALLY COLONIZED THE GASTROINTESTINAL, GENITAL AND URINARY TRACTS. DISEASES IN ADULTS USUALLY FOLLOW WOUND INFECTIONS AND CHILDBIRTH. STARTING TO BE SIGNIFICANT PATHOGEN IN ELDERLY. 60% OF NEW BORNS INOCULATED WITH STRAIN BY PASSAGE THROUGH BIRTH CANAL OR MEDICAL PERSONNEL. DONT CAUSE DISEASE IF MATERNAL ANTI BODIES HAVE PASSED THORUGH PLACENTA. UNINFECTED MOTHERS INCREASE MORTALITY RATES BY 50% |
front 41 GROUP B STREPTOCOCCUS DISEASES | back 41 S. AGALACTIAE CAUSE OF PEURPERAL FEVER/ CHILD BIRTH FEVER ALSO ASSOCIATED WITH: NEONATAL BACTEREMIA, MENINGITIS, AND PNEUMONIA. 25% INFANTS SURVIVING GROUP B STREPTOCOCCAL MENINGITIS HAVE PERMANANENT NEUROLOGICAL DAMAGE, INCLUDING BLINDNESS, DEAFNESS, OR SEVERE MR. ELDERLY ALSO AT RISK 25% DIE FROM STREPTOCOCCAL DISEASES. |
front 42 OTHER BETA HEMOLYTIC STREPTOCOCCI | back 42 S. EQUISIMILIS WHICH CAUSES PHARYNGITIS S. ANGINOSUS PRODUCES PUS CONTAINIG ABSCESSES. PENICILLIN EFFECTTIVE FOR BOTH BOTH ARE ONLY TWO OTHER BETA HEMOLYTIC PATHOGENS |
front 43 ALPHA HEMOLYTIC: THE VIRIDANS GROUP | back 43 PRODUCE A GREEN PIGMENT WHEN GROWN ON BLOOD MEDIA LACK GROUP SPECIFIC CARBOHYDRATES SUSCEPTICIBLE TO PENICILLIN SEPARATE GENUS: ABIOTROPHIA (BY SOME) OTHER NAMES: S. MITIS, S. SANGUIS INHABIT: MOUTH, PHARYNX, GI TRACT, GENITAL TRACT AND URINARY TRACT OF HUMANS |
front 44 ALPHA HEMOLYTIC: THE VIRIDANS GROUP | back 44 ARE OPPORTUNISTS THAT PRODUCE PUS FILLED ABDOMINAL LESIONS ARE ONE CAUSE OF DENTA CARIES STIC K TO DENTAL SURFACES VIA DEXTRAN INSOLUBLE POLYSACCHARIDE COLONIZE WITH OTHER BACTERIA FORMING BIOFILMS ON TEETH ENAMEL KNOWN AS DENTAL PLAQUE IF THEY GET IN BLOOD CAN CAUSE MENINGITIS, AND ENDOCARDITIS |
front 45 STREPTOCOCCUS PNEUMONIAE | back 45 DISCOVERED BY LOUIS PASTEUR IN 1881 IN PNEUMONIA PATIENTS GRAM POSOTOVE COCCUS; 0.5- 1.2 UM IN D FORMS SHORT CHAINS OR MORE COMON PAIRS (DIPLOCOCCUS ONCE CLASSIFIED GENUS) 92 DIFFERENT STRAINS ARE KNOWN TO INFECT HUMANS |
front 46 STREPTOCOCCUS PNEUMONIAE PATHOGENICITY | back 46 NORMAL MEMEBER OF PHARYNGEAL MICROBIOTA THAT CAN COLONIZE LUNGS, SINUSES AND MIDDLE EAR CELSS OF VIRULENT STRAINS SURROUNDED BY POLYSACCHARIDE CAPSULE; PROTECTS FROM DIGESTION OF ENDOCYTOSIS. CAPSULE REQUIRED FOR VIRULENCE CELL WALL CHEMICAL PHOSPHORYLCHOLINE; HIDE IN BODY CELLS CAN PASS INTO THE BLOOD AND THE BRAIN SECRETE PROTEIN ADHESIN |
front 47 STREPTOCOCCUS PNEUMONIAE PATHOGENICITY | back 47 SECRETES 1GA PROTEASE, AND PNEUMOLYSIN PRODUCES TRANSMEMBRANE PORES; RESULTS IN LYSIS OF CELLS PNEUMOLYSIN SUPPRESSES THE DIGESTION OF ENDOCYTIZED BACTERIA INTERFERES WITH LYSOSOMMES ACTION |
front 48 STREPTOCOCCUS PNEUMONIAE EPIDEMIOLOGY | back 48 GROWS IN MOUTHS AND PHARYNGES OF 75% OF HUMANS WITHOUT CAUSING DISEASE WHEN TRAVELED TO LUNGS; CAUSES DISEASE MOST COMMON IN CHILDRENA ND EDERLY |
front 49 PNEUMOCOCCAL DISEASES | back 49 PNEUMOCOCCAL PNEUMONIA CONSTITUTES 85% OF ALL CASES OF PNEUMONIA SINUSITIS AND OTISIS MEDIA BACTEREMIA AND ENDOCARDITIS PNEUMOCOCCAL MENINGITIS |
front 50 ENTEROCOCCUS TWO PATHOGENS TO HUMANS: E. FAECALIS; E. FAECIUM | back 50 GRAM POSITIVE; CATALASE NEGATIVE COCCI SPHERICAL AND LIVE IN INTESTINAL TRACTS OF ANIMALS UNENCAPSULATED TYPICALLY NON HEMOLYTIC FORM SHORT CHAINS AND PAIRS GROW AT TEMPS OF 45C; PH AS HIGH AS 9.6 6.5% SALT/ NACL; OR 40% BILE SALT BROTHS |
front 51 ENTEROCOCCUS PATHOGENESIS, EPIDEMIOLOGY, AND DISEASES | back 51 E. FAECALIS: UBIQUITOUS IN HUMAN COLON BOTH HAVE ABIITY TO ADHERE TO EPITHELIAL CELLS , AND SECRETE BACTERIOCINS WHICH INHIBIT GROWTH OF OTHER BACTERIA CAN CAUSE SERIOUS DISEASE F THEY ARE INTRODUCED TO OTHER PARTS OF THE BODY SUCH AS LUNGS, URINARY TRACT, AND BLOODSTREAM ACCOUNT FOR 10% NOSOCOMIAL INFECTIONS; AND CAUSE BACTEREMIA, ENDOCARDITIS AND WOUND INFECTIONS.. |
front 52 BACILLUS | back 52 GRAM POSITIVE BACILLUS DIVIDED INTO ENDOSPORE FORMING AND NON ENDOSPORE FORMING GENERA ENDOSORE FORMING ARE: BACILLUS AND CLOSTRIDIUM |
front 53 BACILLUS ANTHRACIS | back 53 ROD SHAPED; FACULTATIVELY ANAEROBIC ENDOSPORE FORMING; NORMALLY DWELL IN SOIL SINGLY, PAIRED OR IN CHAINS CAN SURVIVE FOR CENTURIES HAS ANTHRAX TOXINS |
front 54 BACILLUS ANTHRACIS EPIDEMIOLOGY | back 54 PRIMARILY A DISEASE OF HERBIVORES; HUMANS CONTRACT FROM INFECTED ANIMALS CAN IN VADE IN ONE OF THREE ROUTES: INHALATION OF ENDOSPORES, INGESTION OF ENDOSPORES, AND INOCULATION OF ENDOSPORES THROUGH BREAK INT HE SKIN |
front 55 BACILLUS ANTHRACIS DISEASE | back 55 CAUSES ONLY ONE DISEASE - ANTHRAX CAN HAVE THREE CLINICAL MANIFESTATIONS; GASTROINTESTINAL ANTHRAX, INTESTINAL HEMORRHAGING, DEATH CUTANEOUS ANTHRAX - CREATES ESCHARS- RELEASES ANTHRAX TOXIN IN THE BLOOD AND PRODUCES TOXEMIA INHALATION ANTHRAX. SECRETE TOXINS IN LUNGS THAT ARE ABSORBED IN THE BLOOD STREAM. PRODUCING TOXEMIA. IF CAUGHT LATE MORTALITIY RATE IN NEAR 100% |
front 56 CLOSTRIDIUM | back 56 ANAEROBIC; GRAM POSITIVE ENDOSPORE FORMING BACILLUS IN SOIL, WATER, SEWAGE, GI TRACT OF ANIMALS AND HUMANS PATHOGENICITY S DUE TO ENDOSPORE BEING ABLE TO SURVIVE HARSH CONDITIONS SECRETES HYSTOLYTIC TOXINS, ENTEROTOXINS AND NEUROTOXINS MOST COMMON: C. PERFRINGENS, C. DIFFICILE, C. BOTULINUM, AND C. TETANI |
front 57 CLOSTRIDIUM PERFRINGENS PATHOGENESIS, EPIDEMIOLOGY, AND DISEASE | back 57 LARGE ALMOST RECTANGULAR GRAM POSITIVE BACILLUS C. PERFRINGENS TYPE A IS MOST VIRULENT SEROTYPE PRODUCES 11 TOXINS THAT LYSE ENTHROCYTES, AND LEUKOCYTES; INCREASE VASCULAR PERMEABILITY, REDUCE BLOOD PRESSURE AND KILL CELLS RESULTING IN IRREVERSIBLE DAMAGE. SEVERITY RANGES FROM MILD FOOD POISONING TO LIFE TREATENING ILLNESS |
front 58 CLOSTRIDIUM PERFRINGENS PATHOGENESIS, EPIDEMIOLOGY, AND DISEASE | back 58 FOOD POISONING IS BENIGN RESUTS ARE ABDOMINAL CRAMPA, WATERY DIARRHEA, NO FEVER OR NAUSEA OR VOMITING IT IS NOT INVASISVE BUT WHEN INTRODUCED BY SOME TRAUMATIC EVENT ( GUN SHOT, PUNCTURE ETC) CAB GERMINATE IN DEEP TISSUE CLOSTRIDIAL TOXINS INDUCE SWELLING AND TISSUE DEATH RAPIDLY REPRODUCING BACTERIA CAN SPREAD INTO SURROUNDING TISSUE ACCOMPANIED BY PRODUCTION OF FOUL SMELLING, GASEOUS, BACTERIAL WASTE PRODUCTS -- GAS GANGRENE SHOCK, KIDNEY FAILURE AND DEATH CAN FOLLOW WITHIN A WEEK OF INFECTION |
front 59 GAS GANGRENE TREATMENT C. PERFRINGENS | back 59 DEAD TISSUE AFFECTED BY GAS GANGRENE HAS TO QUICKLY BE SURGICALLY REMOVED AND BY LARGE DOSES OF ANTITOXIN AND PENICILLIN. OXYGEN APPLIED UNDER PRESSURE MAY ALSO BE HELPFUL MORTALITY RATE WITH TREATMENT EXCEEDS 40% REFRGERATION PREVENTS TOXIN FORMATION AND REHEATING DESTROYS TOXIN THAT HAS FORMED AS WELL AS PROPER CLEANING OF WOUNDS |
front 60 CLOSTRIDIUM DIFFICILE | back 60 MOTILE, ANAEROBIC INTESTINAL BACTERUIM ABOUT 1.5 UM IN WIDTH; 3-6.5 UM IN LENGTH FORMS OVAL SUBTERMINAL ENDOSPORES PRODUCES TWO TOXINS A & B; ENZYME HYALURONIDASE |
front 61 CLOSTRIDIUM DIFFICILE PATHOGENESIS, EPIDEMIOLOGY, AND DISEASE | back 61 IT IS AN OPPORTUNISTIC PATHOGEN AND IS A RESIDENT IN MICROBIOTA OF INTESTINE NORMAL PROPORTIONS OF DIFFERENT BACTERIA IN COLON ARE SIGNIFICANTLY ALTERED HARDY ENDOSPORES GERMINATE ENABLING IT TO BECOME PREDOMINATE INTESTINAL BACTERIUM TOXINS AND ENZYMES IT PRODUCES HEMORRHAGIC DEATH OF INTESTINAL WALL CAN PRODUCE LIFE THREATENING PSEUDOMEMBRANOUS COLITIS- LARGE SECTIONS OF COLON SLOUGH OFF MAJOR CAUSE OF ELDERLY DEATH |
front 62 CLOSTRIDIUM BOTULINUM | back 62 ANAEROBIC, ENDOSPORE FORMING, GRAM POSITIVE BACILLUS COMMON IN SOIL AND WATER WORLD WIDE ENDOSPORES CAN SURVIVE IMPROPER CANNING OF FOOD CAN PRODUCE POWERFUL NEUROTOXIN THAT CAUSES BOTULISM |
front 63 CLOSTRIDIUM BOTULINUM PATHOGENESIS | back 63 PRODUCE ON OF SEVEN ANTIGENICALLY DISTINCT BOTULISM TOXINS (A THROUGH G) CONSIDERED ONE OF DEADLIEST TOXINS KNOWN- 30 GRAMS WOULD BE ENOUGH TO KILL EVERY PERSON IN THE U.S. EACH OF SEVEN TOXINS IS A QUATERNARY PROTEIN BOTULISM TOXINS ACT BY BINDING IRREVERSIBLY TO NEURONAL CYTOPLASMIC MEMEBRANES, PREVENTING FUSION OF VESICLES AND SECRETION OF ACETYLCHOLINE INTO THE SYNAPTIC CLEFT. PREVENTS MUSCLE CONTRACTION RESULTING IN FLACCID PARALYSIS |
front 64 CLOSTRIDIUM BOTULINUM EPIDEMIOLOGY AND DISEASES | back 64 BOTULISM IS NOT AN INFECTION ITS AN INTOXICATION CAUSED BY BOTULISM TOXIN. THREE MANIFESTATIONS: FOODBORNE BOTULISM, INFANT BOTULISM, AND WOUND BOTULISM |
front 65 CLOSTRIDIUM BOTULINUM TREATMENT | back 65 THREE APPROACHES: REPEATED WASHING OF THE INTESTINAL TRACTTO REMOVE CLOSTRIDIUM ADMINISTRATION OF ANTIBODIES AGAINST BOTULISM TOXIN TO NEUTRALIZE TOXIN IN THE BLOOD BEFORE IT CAN BIND TO NEURONS ADMINISTRATION OF ANTIMICROBIAL DRUGS TO KILL CLOSTRIDIA IN INFANT AND WOUND BOTULISM CASES |
front 66 CLOSTRIDIUM TETANI | back 66 SMALL MOTILE OBLIGATE ANAEROBE, THAT PRODUCES A TERMINAL ENDOSPORE, GIVING CELL A DISTINCTIVE LOLLIPOP APPEARANCE IN SOIL, DUST AND GI TRACT OF ANIMALS AND HUMANS EXTREMELY SENSITIVE TO OXYGEN TOXIN CAUSES DISEASE TETANUS |
front 67 CLOSTRIDIUM TETANI PATHOGENESIS | back 67 TETANOSPASMIN (TETANUS TOXIN) POTENT NEUROTOXIN RELEASED WHEN C. TETANI CELLS DIE. ITS COMPOSED OF TWO POLYPEPTIDES HELD TOGETHER BY A DISULFIDE BOND. BLOCKS THE RELEASE OF INHIBITORY NEUROTRANSMITTER . WITH BLOCKAGE EXCITATORY ACTIVITY IS UNREGULATED, MUSCLES SIGNALED TO CONTRACT SIMULTANEOUSLY MUSCLES ON BOTH SIDES OF JOINT DONT RELAX CONTRACTION CAN BE SO SEVERE THEY BREAK BONES |
front 68 CLOSTRIDIUM TETANI EPPIDEMIOLOGY, DISEASE | back 68 INCUBATION PERIOD IS A FEW DAYS TO A WEEK INITIAL SIGN IS TIGHTENING OF NECK AND JAW MUSCLES - LOCKJAW OTHER SYMPTOMS: SWEATING, DROOLING, GROUCHINESS, AND CONSTANT BACK SPASMS, CAN SPREAD AND CAUSE HEART BEAT IRREGULARITIES, FLUCTUATIONS IN BLOOD PRESSURE, EXTENSVE SWEATING UNRELENTING CONTRACTION OF DIAPHRAGM RESULT IN FINAL INHALATION; CANT EXHALE; DEATH MORTALITY RATE 50%; NEONATAL TETANUS IS 90% UMBILICAL STUMP |
front 69 LISTERIA MONOCYTOGENES | back 69 LLOW G+C, GRAM POSITIVE NON EDOSPORE FORMING BACILLUS FOUND IN SOIL, WATER, MAMMALS, BIRDS FISH, AND INSECTS ENTERS THE BODY IN CONTAMINATED FOOD AND DRINK |
front 70 LISTERIA MONOCYTOGENES PATHOGENESIS, EPIDEMIOLOGY, DISEASE | back 70 BINDS TO SURFACE OF MACROPHAGE OR A CELL OF THE LIVER OR GALL BLADDER. TRIGGERS ITS OWN ENDOCYTOSIS TO BECOME A FACULTATIVE INTRACELLULAR PARASITE SYNTHESIZES PORE FORMING PROTEIN- LISTERIOLYSIN O (PUNCTURES PHAGOSOME MEMBRANE) RELEASING BACTERIUM INTO HOST CELLS CYTOSOLE; BEFORE LYSOSOME CAN FUSE PHAGOSOME. CAN TRANSFER ITSELF WITHOUT HAVING TO LEAVE HOST CELL FORMS A PSEUDOPOD VIRULENCE DIRECTLY RELATED TO ABILTY T LIVE IN CELLS |
front 71 LISTERIA MONOCYTOGENES PATHOGENESIS, EPIDEMIOLOGY, DISEASE | back 71 PRODUCES NO TOXINS OR ENZYMES THAT MAKE IT VIRULENT BACTERIUM ONLY PRODUCES RAPIDLY WHEN IN A HOST (37C) LITTLE T NO EFFECT ON HEALTHY ADULTS SEVERE EFFECT ON: FETUSES, NEWBORNS, ELDERLY AND IMMUNOCOMPROMISED PATIENTS IN THESE PATIENTS LISTERIA TRAVELS VIA BLOODSTREAM TO BRAIN CAUSING MENINGITIS AND POSSIBLY DEATH. LOW TEMPS DO NOT INHIBIT BACTERIA |
front 72 MYCOPLASMAS | back 72 SMALLEST FREE LIVIING MICROBES THAT CAN GROW AND REPRODUCE INDEPENDENTLY OF OTHER CELLS. STAIN PINK, HAVE NO CELL WALLS FACULTATIVE ANAEROBES COLONIES HAVE FRIED EGG APPEARANCE MYCOPLAMA PNEUMONIAE CAUSES PRIMARY ATYPICAL PNEUMONIA (WALKING PNEUMONIA) MYCOPLASMA HOMINIS CAN CAUSE PID MYCOPLASMA GENITALIUM CAN CAUSE NONGONOCOCCAL URETHRITIS |
front 73 CORYNEBACTERIUM DIPTHERIAE | back 73 TRANSMITTED VIA RESPIARTORY DROPLETS CONTAINS A BACRIOPHAGE THAT CODES FOR DIPHTHERIA TOXIN, WHICH CAUSES SYMPTOMS FOR POTENTIALLY FATAL DISEASE DIPHTHERIA DIAGNOSED BY THE ELEK TEST |
front 74 MYCOBACTERIUM | back 74 HIGH G+C, NON ENDOSPORE FORMING PATHOGEN HAVE AN ABUNDANCE OF WAXY LIPID/ MYCOLIC ACID IN CELL WALL GROWS SLOWLY GENERATION TIME VARIES FORM HOURS TO SEVERAL DAYS PROTECTED FROM LYSIS ONCE PHAGOCYTIZED CAPABLE OF INTRACELLULAR GROWTH RESISTANT TO GRAMM STAINING, DETERGENTS, MANY ANTIMICROBIAL DRUGS AND DESICCATION ACID FAST STAIN PATHOGENIC TYPES: M. TUBERCULOSIS, M. LEPRAE; M. AVIUM-INTRACELLULARE AND M. ULCERANS CAUSE EMERGING MYCOBATERIAL DISEASES |
front 75 MYCOBACTERIUM TUBERCULOSIS | back 75 PRIMARY MYCOBACTERIAL DISEASE GROWN ON DUL YELLOW AGAR CALLED LOWENSTEIN -JENSEN AGAR VIRULENT STRAINS HAVE A CELL WALL COMPONENT - CORD FACTOR PRODUCES DAUGHTER CELLS THAT REMAIN ATTACHED IN PARALLEL ALIGNMENTS INHIBITS MIGRATION OF NEUTROPHILS; TOXIC TO MAMMAL CELLS |
front 76 MYCOBACTERIUM TUBERCULOSIS PATHOGENESIS AND DISEASE | back 76 WAXY WALL PROTECTS FROM DISSECATION CAN REMAIN VIABLE IN DRIED AEROSOL DROPLETS FOR 8 MONTHS NOT TO VIRULENT; ONLY 5% INFECTED DEVELOP DISEASE KILLS 50% OF UNTREATED PATIENTS 3 TYPES: PRIMARY, SECONDARY, DISSEMINATED |
front 77 PRIMARY TUBERCULOSIS | back 77 PRIMARY TB TYPICALLY OCCURS IN CHILDREN, INVOLVES FORMATION OF SMALL HARD NODULES IN LUNGS- TUBERCLES STAGES: 1. IN HALATION OF RESPIRATORY DROPLETS; MINIMUM INFECTIOUS DOSE IS 10 CELLS, HAVE ADHESIVE PILI THAT ATTACH TO LAMININ 2. MACROPHAGES IN THE AVEOLI OF LUNGS PHAGOCYTIZE PATHOGENS BT ARE UNABLE TO DIGEST THEM. IT INAVDES CELLS LINING AVEOLI 3. REPLICATE FREELY WITHIN HOST CELLS, KILLING THEM. INFECTED CELLS RELEASE CHEMOKINES AND ATTRACT MORE MICROPHAGES, BACTERIA RELEASED FROM DEAD MACROPHAGES GET PHAGOCITIZED BY NEW MACROPHAGES BEGINNING CYCLE ANEW. 4. LIGHTLY APPRESSED MACROPHAGES SURROUND THE SIGHT OF INFECTION FORMING A TUBERCLE 5. INFECTED CELLS IN THE CENTER OF THE TUBERCLE DIE, RELEASING M. TB AND PRODUCING CASEOUS NECROSIS TUBERCLE FILLED WITH AIR CALLED TUBERCULOUS CAVITY GHON COMPLEXES- CALCIUM DEPOSITS AROUND THE TUBERCLES |
front 78 SECONDARY TUBERCULOSIS | back 78 RESULTS WHEN M. TB BREAKS THE STALEMATE, RUPTURES THE TUBERCLE AND REESTABLISHES AN ACTIVE INFECTION IN WHICH BACTERIA SPREAD THROUGH THE LUNGS VIA THE BRONCHIOLES |
front 79 DISSEMINATED TUBERCULOSIS | back 79 RESULTS WHEN SOME MACROPHAGES CARRY THE PATHOGENS VIS THE BLOOD AND LYMPH TO A VARIETY OF SITES, INCLUDING: BONE MARROW, SPLEEN. KIDNEYS, SPINAL CORD AND BRAIN OLD NAME- CONSUMPTION |
front 80 MYCOBACTERIUMTUBERCULOSIS EPIDEMIOLOGY | back 80 PANDEMIC IN OTHER PARTS OF THE WORLD KILLING 2 MILLION ANNUALLY 1/3 WORLD POPULATION INFECTED WITH M T.B. AND 10% DEVELOP LIFE THREATENING CASE RISK FACTORS INCLUDE: DIABETES, POOR NUTRITION, STRESS, CROWEDED LIVING CONDITIONS, ALCOHOL AND DRUG ABUSE AND SMOKING |
front 81 MYCOBACTERIUM TUBERCULOSIS DIAGNOSIS TREATMENT AND PREPVENTION | back 81 TUBERCULIN SKIN TEST USED TO SCREEN PATIENTS FOR POSSIBLE EXPOSURE;HARD RED SWELLING AT TEST SITE 24-72 HRS LATER IS POSITIVE DOESNT INDICATE CURRENT DISEASE CHEST XRAYS USED TO REVEAL TUBERCLES IN LUNGS (PRIMARY IN LOWER LUNGS AND SECONDARY HIGHER IN LUNGS) MDR-TB AND XDR-TB (MULTI DRUG RESISTANT; EXTENSIVELY DRUG RESISTANT TB) BCG VACCINE NOT WARRANTED IN THE U.S. |
front 82 MYCOBACTERIUM LEPRAE | back 82 CAUSES LEPROSY TUBERCULOID LEPROSY IS A NON PROGRESSIVE FORM OF THE DISEASE LEPROMATOUS LEPROSY RESULTS IN PROGRESSIVE DESTRUCTION OF BODY STRUCTURES |
front 83 NARCADIA AND ACTINOMYCES | back 83 OPPORTUNISTIC PATHOGEN NARCADIA ASTEROIDES HAS ELONGATED CELLS RESEMEBLING FUNGAL HYPHAE ITS ACID FAST BECAUSE OF PRESENCE OF MYCOLIC ACID IN CELL WALL CUTANEOUS INFECTIONS MAY PRODUCE MYCETOMA ACTINOMYCES - ANOTHER OPPORTUNISTIC PATHOGEN WITH ELONGATED CELLS, NOT ACID FAST; CAUSES ACTINOMYCOSIS. |