-Gram positive cocci (purple)

-Pairs and chains

-Facultative anaerobes

-Normal flora of skin, mucous membranes, mouth and pharynx

-18 Lancefield grps: A-H and K-T (based on type of carbohydrate "c" in cell wall and specific for each grp)

ALPHA: partial breakdown of RBCs in agar (partial clearing), greenish color

BETA: complete breakdown of RBCs in agar (complete clearing)

GAMMA: No RBC breakdown (no clearing)

Group A Strep:

Strep pyogenes

Identification: Beta hemolytic, Lancefield grp A, Bacitracin sensitive, SXT resistant

Infections: strep throat, tonsillitis, erysipelas (contagious skin infection), impetigo, septicemia, pneumonia, others

Post-strep diesases: antigen on beta strep grp A resembles heart valves and glomerulus which cross-react and cause rheumatic fever and glomerulonephritis

Grp A Strep:

Enzymes/Toxins

Streptolysin O - oxygen kills it, can only hemolysize in anaerobic cond. and since culture in aerobic, won't see hemolysis

Streptolysin S - oxygen stable, hemolysis in either aerobic/anaerobic cond.

Erythogenic toxin - rash of scarlet fever, toxin is absorbed/carried by blood

Streptokinase/Fibrinolysin - break down fibers, helps org. spread

Hyaluronidase - breaks down hyaluronic acid (binds connective fibers)

Exotoxins - do a variety of things, fever, shock...

Normal flora in vajayjay and oral cavity

Infections: meningitis/septicemia in newborns, post-partum women, female urinary/genital tract, wound/skin

Identification: beta hemolytic, Lancefield grp B, CAMP test (CAMP factors enhance hemolytic reaction of S. aureus

Penicillin sensitive

Bile esculin positive

NaCl negative

Penicillin resistant

Bile esculin positive

NaCl positive

Vancomycin-resistant Entero. (VRE):

usually sensitive to aminoglycoside (gpc), not VRE, screen w/vanc agar plates, nosocomial infections

General Chars: Gram positive diplococci, common mouth/pharynx flora, need increase in CO₂, alpha hemolytic, lysed by bile salts (colonies broken down by bile salts), optochin sensitive

Infections: pneumonia, meningitis, septicemia, pericarditis, pleuritis, otitis media

Can be isolated from any anatomical site, major cause of nosocomial infections, commonly found in GI track, water/dirt samples

Chars: Gram negative rods, aerobic/facultative anaerobes, some are motile, fermenters of glucose and use pyruvic acid as final acceptor instead of O₂, oxidase negative, non spore forming

Contains bile salts/crystal violet which inhibit GPC

Lactose/neutral red dye serve as pH indicators

Lactose fermenters produce mixed acid and change red to bright pink

Lactose indicators do not utilize lactose and colonies clear

Determine enzyme tryptophanase (indole + pyruvic acid + ammonia)

Add Kovac's reagent

Results must be read within 15 mins

Positive: forms red ring at surface

Negative: no red ring

Indicates type of glucose fermentation called mixed acid fermentation which makes a lot of acidic products thus lowering pH

Add methyl red, turns red @ acidic pH

Positive: red color present

Negative: yellow/orange color

Indicates form of glucose ferm. called butanediol ferm. which makes neutral products/acetyl methyl carbinol

Add Barritt's reagent A, then Barritt's reagent B which detects acetyl methyl carbinol

Results must be read after 30 min

Positive: pink, orange OR red layer

Negative: no pink...

Medium contains citrate as only usable carbon source

Contains pH indicator bromthymol blue (Green = neutral pH, Blue = basic pH)

Bacteria must contain transport enzyme for citrate, if it does use the citrate alkaline products will be formed

Positive: BLUE

Negative: Green, no blue

Detects production of urease, breaks down urea into ammonia and CO₂

Medium contains indicator phenol red, which turns pink in basic cond.

Positive: Pink

Negative: not pink

Detects ferm. of glucose and lactose

Detects production of H₂S and CO₂

Look at both slant and butt colors (slant/butt)

Red = alkaline (K), no ferm.

Yellow = acidic (A), ferm.

Glucose ferm ONLY: K/A

Glucose AND lactose ferm: A/A

Non-ferm: K/K

Detects mobile bac.

Stab media

Positive: bac. grow out from stab line

Negative: bac. only grow in stab line

Indole negative

Methyl red negative

VP positive

Citrate positive

Urea negative

Indole positive

Methyl red positive

VP negative

Citrate negative

Urea negative

Indole negative

Methyl red negative

VP positive

Citrate positive

Urea positive

Indole negative

Methyl red positive

VP negative

Citrate negative

Urea positive

Indole positive

Methyl red positive

VP negative

Citrate negative

Urea positive

Gastroenteritis

Inflammation of stomach/intestine lining

May be accompanied by severe pain

Caused by enterotoxins released by bac. which disrupt epithelial cells of small intestine

This causes increased secretion of electrolytes/water loss (secretory diarrhea)

Bac. don't actually invade tissue, but toxins do damage it

Large stool volume, little blood

cholera, some E. coli and shigella

exotoxins made by GPC/GNR

Orgs. invade wall of intestines, disrupt architecture leading to gross injury

Smaller fecal volume, blood, ulceration of inner mucosal lining

salmonella, some E. coli and campylobacter

Leading cause of infant mortality

In some areas 15-25% of children die by age 5

Higher infection rates in tropical regions w/poor water sanitation

Urging 3rd world mothers to breast feed

ferments lactose, most commonly isolated orgs. in clinical specimens, isolated from almost every human tissue/organ

-sepsis

-endotoxins induced shock

-urinary tract/wound infections

pneumonia in immuno-compromised patients

meningitis (babies)

Toxigenic

Produce enterotoxin that causes secretory diarrhea

Traveler's diarrhea, Montazuma's revenge, Delhi belly

Local population of regions have developed immunity to bacteria in their water

Symptoms within 5-15 days

Pepto-Bismol

Bac. must attach to surface of intestinal epithelials for toxin production

Invasive

Pathogenesis unclear, causes diarrheal syndromes mostly in kids, inflammatory rxn to break down of intestinal epith.

Invasive

Feces contain blood, mucous and white blood cells

Bac. penetrate intestinal epith. causing inflammatory diarrhea

Enterhemorrhagic E. coli (EHEC)

or

Verotoxin producing E. coli (VTEC)

Toxigenic

Bloody diarrhea due to toxins' damage of epith. cells

Associated with:

hemorrhagic colitis: present w/abdominal cramps/watery diarrhea then bloody diarrhea, no significant fever/WBCs in stool

and hemolytic uremic syndrome: leading cause of acute renal failure in kids, present with diarrheal illness that becomes bloody, only type of E. coli that is sorbitol negative (isolated using MAC w/sorbitol instead of lactose) clear colonies

Do not ferment lactose

tend to be biochemically inert

fecal/oral route: only takes about 100 orgs to cause sickness, common in daycares

toxigenic only

course of illness shigellosis: endotoxin causes fever, enterotoxin causes inflammation/degeneration of intestinal wall

increased fluid loss: fever, watery diarrhea/cramping, general pain, electrolyte loss

After 2-3 days: bowel movements become less frequent and quantity of stools increase, still RBCs and mucous in feces

Most associated w/diarrheal disease

Symptoms tend to be mild/asymptomatic

Least commonly recovered

Most virulent: produces exotoxin that acts on blood vessels of brain (shiga toxin), may lead to neurological symptoms (cause coma)

Main reservoirs in nature are reptiles

Does NOT ferment lactose

Produces a lot of hydrogen sulfide (TSI)

E. tarde - wound infections resulting from trauma (aquatic accidents), gastroenteritis that improves w/out therapy, not known to cause diarrhea

Do NOT ferment lactose

Produce a little hydrogen sulfide

Infections caused by contaminated food/water/milk (contaminated by humans/chickens/rats/turtles...)

Primary pathogen of lower animals (cows, pigs, pets) - principle source of non-typhoidal Salmonella infections caused by S. typhimunum and S. enteritidis

Usually recover spontaneous/do not require tx

Humans only known reservoir of S. typhi - causes typhoid fever, can carry but not show symptoms, infection takes 200,000-1 mil. bac.

epithelial cells lining of small intestines, invasive infection that leads to septicemia - causes ulceration of intestines, invades lymph nodes and liver/spleen network

Can hide in gall bladder for years and be shed, causing infection

Approx. 450 cases/yr in US

Fever, severe headache, abdominal pain

Intestines may rupture - bleeding/shock

1 in 5 die if not treated

Person w/previous S. typhi infection can carry bacteria in their feces

Gastroenteritisis: most common, mild-bad diarrhea, low fever, varying degrees of N/V, infection takes 2-3 days to colonize

Septicemia: high spiking fever, positive blood culture

Enteric fever: mild fever/diarrhea

Natural habitat: soil, water, human feces

Can cause UTI/septicemia in debilitated patients

Associated w/memingitis/brain abcesses in neonates

Large colonies of mucoid consistency

Lactose positive

Urea positive

Widely dist. in nature/GI tract of humans/animals

Lung infections in debilitated patients (alcoholism/diabetes)

Enteritis/meningitis in infants

UTI in children/adults

Septicemia

Klebsielleae: Enterobacter: E. aerogenes

and

E. cloacae

Widely dist. in water, sewage, soil, veg

Normal enteric flora of intestines

Not known to cause diarrhea

Associated w/opportunistic infections: UTI, respiratory tract, cutaneous wounds, occasional septicemia/meningitis

occur naturally in soil/water

normal flora of intestines

S. marcescens most common-

intense red pigment, 18th century appeared on surfaces of communion wafers (thought it was blood = miracle), used to trace air currents in hospitals which now realize it is an important pathogen

Assoc. w/pneumonia and septicemia in chemo patients, nosocomial opportunist, found in burn/wound infections

Soil, water, fecal matter

swarming motility (wavelike spreading across surface of agar)

P. mirabilis - UTI/wound infections, Indole negative

P. vulgaris - infected sites of immuno-supressed host, Indole positive

The Plague:

Y. pestis

Found in rodents, transferred via rat flea

3 Forms:

Bubonic plague

Septicemia plague

Pneumonic plague

Fatality if untreated: 50-75% for bubonic, almost 100% for septicemic and pneumonic

Treated: has 90-95% survival rate

Diagnosis and Tx: death may occur 2-4 days

1 of 4 internationally quarantinable diseases:

Plague

Smallpox

Cholera

Yellow Fever

bacteria multiply in flea bite, then enter lymph system

causes inflammatory swelling of lymph nodes: called Bubo, typically in groin, occasionally in neck/axilla, incubation period is 2-8 days, abrupt ending w/onset of fever, chills, headache, nausea, weakness and extreme tenderness of bubo

Bubonic plague progresses to massive bac. growth in blood caused by: disseminated intravascular coagulation which initiates clotting mechanisms, circulatory stagnation and subcutaneous hemorrhage

Purpura that may degenerate into necrosis/gangrene - bleeding into skin/mucosa, appear as patches of red that turn purple/black giving it the name "black death"

Dreaded complication

infection lodged in lungs

highly contagious