GRAM POSITVE BACTERIA

STAIN PURPLE WHEN GRAM STAINED

FALL INTO PHYLUM FIRMICUTES

TWO MAJOR GROUPS: LOW G+C GRAM POSITIVE AND HIGH G+C GRAM POSITIVE

STAPHYLOCOCCUS (GENUS)

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

STAPHYLOCOCCUS

GRAM POSITIVE

FACULTATIVE ANAEROBES; PROKARYOTIC

SPHERICAL CELLS ARE CLUSTERED IN GRAPELIKE ARRANGEMENTS

CAPABLE IN GROWING IN MEDIA THAT ARE 10% NACL (SALT)

SYNTHESIZES CATALASE

S. AUREUS

S. EPIDERMIDIS

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.

STAPHYLOCOCCUS

PATHOGENICITY

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

STRUCTURAL DEFENSES

(STAPHYLOCOCCUS)

PROTEIN A

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

STRUCTURAL DEFENSES

STAPHYLOCOCCUS

BOUND COAGULASE

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)

ENZYMES

STAPHYLOCOCCUS

(CELL FREE COAGULASE; HYALURONIDASE)

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.

ENZYMES

S. AUREUS

STAPHYLOKINASE, LIPASES (S. AUREUS, S. EPIDERMIDIS)

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.

ENZYMES

S. AUREUS

BETA-LACTAMASE

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

TOXINS

CYTOLYTIC TOXINS

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

TOXINS

EXFOLIATIVE TOXINS

EACH OF TWO DISITNCT PROTEINS CAUSES THE DISSOLUTION OF EPIDERMAL DESMOSOMES CAUSING PATIENTS SKINS CELLS TO SEPARATE FROM EACH OTHERAND SLOUGH OFF OF BODY.

TOXIC SHOCK SYNDROME (TSS) TOXIN

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.

ENTEROTOXINS

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

EPIDEMIOLOGY

S. AUREUS, S. EPIDERMIDIS

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

NONINVASIVE DISEASE

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

CUTANEOUS DISEASES

STAPHYLOCOCCAL SCALDED SKIN SYNDROME

IMPETIGO

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.

CUTANEOUS DISEASES

FOLLICULITIS

STY

FURUNCLE/ CARBUNCLE

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

BACTEREMIA

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.

ENDOCARDITIS

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

PNEUMONIA AND EMPYEMA

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.

OSTEOMYELITIS

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.

DIAGNOSIS OF STAPHYLOCOCCUS

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

MRSA/ VRSA

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

STAPH PREVENTION

PROPER CLEANSING OF WOUNDS AND SURGICAL OPENINGS

ASEPTIC USE OF CATHETERS AND INDWELLING NEEDLES

APPROPRIATE USE OF ANTISEPTICS

HANDWASHING

STREPTOCOCCUS

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)

LANCEFIELD GROUPS

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

GROUP A STREPTOCOCCUS

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

GROUP A STREPTOCOCCUS

PATHOGENICITY (M PROTEIN, HYALURONICACID CAPSULE )

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.

GROUP A STREPTOCOCCUS

PATHOGENICITY

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

GROUP A SREPTOCOCCUS

PATHOGENICITY

TOXINS

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

GROUP A

PATHOGENICITY

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

GROUP A

EPIDEMIOLOGY

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

GROUP A

STREPTOCOCCAL DISEASES

PHARYNGITIS, SCARLET FEVER

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.

GROUP A

STREPTOCOCCAL DISEASES

PYODERMA AND ERYSIPELAS

STREPTOCOCCAL TSS

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.

GROUP A STREPTOCOCCAL DISEASES

NECROTIZING FASCIITIS

RHEUMATIC FEVER

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.

GROUP A STREPTOCCCAL DISEASES

GLOMERULONEPHRITIS

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.

GROUP B STREPTOCOCCUS

S, AGALACTIAE

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.

GROUP B STREPTOCOCCUS

PATHOGENICITY

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

GROUP B STREPTOCOCCUS

EPIDEMIOLOGY

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%

GROUP B STREPTOCOCCUS DISEASES

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.

OTHER BETA HEMOLYTIC STREPTOCOCCI

S. EQUISIMILIS WHICH CAUSES PHARYNGITIS

S. ANGINOSUS PRODUCES PUS CONTAINIG ABSCESSES.

PENICILLIN EFFECTTIVE FOR BOTH

BOTH ARE ONLY TWO OTHER BETA HEMOLYTIC PATHOGENS

ALPHA HEMOLYTIC: THE VIRIDANS GROUP

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

ALPHA HEMOLYTIC: THE VIRIDANS GROUP

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

STREPTOCOCCUS PNEUMONIAE

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

STREPTOCOCCUS PNEUMONIAE

PATHOGENICITY

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

STREPTOCOCCUS PNEUMONIAE

PATHOGENICITY

SECRETES 1GA PROTEASE, AND PNEUMOLYSIN

PRODUCES TRANSMEMBRANE PORES; RESULTS IN LYSIS OF CELLS

PNEUMOLYSIN SUPPRESSES THE DIGESTION OF ENDOCYTIZED BACTERIA

INTERFERES WITH LYSOSOMMES ACTION

STREPTOCOCCUS PNEUMONIAE

EPIDEMIOLOGY

GROWS IN MOUTHS AND PHARYNGES OF 75% OF HUMANS WITHOUT CAUSING DISEASE

WHEN TRAVELED TO LUNGS; CAUSES DISEASE

MOST COMMON IN CHILDRENA ND EDERLY

PNEUMOCOCCAL DISEASES

PNEUMOCOCCAL PNEUMONIA CONSTITUTES 85% OF ALL CASES OF PNEUMONIA

SINUSITIS AND OTISIS MEDIA

BACTEREMIA AND ENDOCARDITIS

PNEUMOCOCCAL MENINGITIS

ENTEROCOCCUS

TWO PATHOGENS TO HUMANS:

E. FAECALIS; E. FAECIUM

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

ENTEROCOCCUS

PATHOGENESIS, EPIDEMIOLOGY, AND DISEASES

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..

BACILLUS

GRAM POSITIVE BACILLUS DIVIDED INTO ENDOSPORE FORMING AND NON ENDOSPORE FORMING GENERA

ENDOSORE FORMING ARE: BACILLUS AND CLOSTRIDIUM

BACILLUS ANTHRACIS

ROD SHAPED; FACULTATIVELY ANAEROBIC

ENDOSPORE FORMING; NORMALLY DWELL IN SOIL

SINGLY, PAIRED OR IN CHAINS

CAN SURVIVE FOR CENTURIES HAS ANTHRAX TOXINS

BACILLUS ANTHRACIS

EPIDEMIOLOGY

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

BACILLUS ANTHRACIS

DISEASE

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%

CLOSTRIDIUM

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

CLOSTRIDIUM PERFRINGENS

PATHOGENESIS, EPIDEMIOLOGY, AND DISEASE

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

CLOSTRIDIUM PERFRINGENS

PATHOGENESIS, EPIDEMIOLOGY, AND DISEASE

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

GAS GANGRENE TREATMENT

C. PERFRINGENS

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

CLOSTRIDIUM DIFFICILE

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

CLOSTRIDIUM DIFFICILE

PATHOGENESIS, EPIDEMIOLOGY, AND DISEASE

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

CLOSTRIDIUM BOTULINUM

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

CLOSTRIDIUM BOTULINUM

PATHOGENESIS

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

CLOSTRIDIUM BOTULINUM

EPIDEMIOLOGY AND DISEASES

BOTULISM IS NOT AN INFECTION ITS AN INTOXICATION CAUSED BY BOTULISM TOXIN.

THREE MANIFESTATIONS: FOODBORNE BOTULISM, INFANT BOTULISM, AND WOUND BOTULISM

CLOSTRIDIUM BOTULINUM

TREATMENT

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

CLOSTRIDIUM TETANI

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

CLOSTRIDIUM TETANI

PATHOGENESIS

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

CLOSTRIDIUM TETANI

EPPIDEMIOLOGY, DISEASE

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

LISTERIA MONOCYTOGENES

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

LISTERIA MONOCYTOGENES

PATHOGENESIS, EPIDEMIOLOGY, DISEASE

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

LISTERIA MONOCYTOGENES

PATHOGENESIS, EPIDEMIOLOGY, DISEASE

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

MYCOPLASMAS

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

CORYNEBACTERIUM DIPTHERIAE

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

MYCOBACTERIUM

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

MYCOBACTERIUM TUBERCULOSIS

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

MYCOBACTERIUM TUBERCULOSIS

PATHOGENESIS AND DISEASE

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

PRIMARY TUBERCULOSIS

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

SECONDARY TUBERCULOSIS

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

DISSEMINATED TUBERCULOSIS

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

MYCOBACTERIUMTUBERCULOSIS

EPIDEMIOLOGY

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

MYCOBACTERIUM TUBERCULOSIS

DIAGNOSIS TREATMENT AND PREPVENTION

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.

MYCOBACTERIUM LEPRAE

CAUSES LEPROSY

TUBERCULOID LEPROSY IS A NON PROGRESSIVE FORM OF THE DISEASE

LEPROMATOUS LEPROSY RESULTS IN PROGRESSIVE DESTRUCTION OF BODY STRUCTURES

NARCADIA AND ACTINOMYCES

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.