Test on exam 2 – Microbiology Flashcards

staphylcoccus aureus

staphylcoccus epidermidis

staphylcoccus saprophyticus

gram pos cocci

arrangement-irregular clusters

non spore formers

non motile

usually no capsule with the exeption of staphylcoccus aureus which has a capsule

toxins

enzymes

structural compenents
toxins and enzymes are both extracellular

hemolysin

leukocidin

enterotoxin

toxic shock syndrome (TSST-1)

lyses white blood cells by disrupting cell membrane

incapacitates the host's immune response

coagulase

fibrinolysin

hyaluronidase

lipase

penicillinase

catalase

exofoliatin or epidermoyltic toxin

plasma clotting protein; converts fibrinogen to fibrin

coats bacteria w/ fibrin and prevents phagocytosis

aids in attachment

digests fibrinogen (fibrin clots)

normally fibrogen is converted to firbin by coagulase (and the subsequent fibrin makes a clot)

clot on exterior surface inhibits phagocytosis and helps in attachment

spreading factor

digers hyaluronic acid (cememnt b/w cells) around host cells which promotes invasion and allows it to move from focal pt to other parts

degrades lipids

allows bacteria to colonize on oily skin

hydrolyzes penicillin

drug resistance

inactivates peniciate-what gorohea does

degrades H2O2 (hydrogen peroxide)

toxic metabolite end product

structural surgace component virulence factor

surface component linked to peptidoglycan of call wall (of staph aureus); inhibits antibody mediated clearance of bacteria by binding to IgG (completes for IgGs binding site)

binds to tissue components; cell adhesion

considered structural surface component in staph

coagulase positive

hemolysin (alpha toxin)

leukocidin

protein A

capsule

**Most resistant of all non spore formers

major pathogen of genus

carriage location-anterior nares, nasopharynx, skin

carriage rate-30 to 50 % of healthy adults

blood cell toxins

intestinal toxins

epithetlial toxins

hemolysins-hemolytic, have a clearing around the colony

leukocidins

exofoliatin or epidermolytic toxin

superficial peeling of skin

superficial infections

toxigenic infections

systemic infections

staphylococcal scalded skin syndrom (SSSS)

pyodermic infections

pimples, boils, carbuncles, and impetigo

pus formation,edema, pain, erythema, infection site has an absess formed (localized inflammatory reac-fibrin clot stops infection from spreading)

staphlococcus-pyogenic cocci

primary infection sites at face, back of neck, buttocks

risk groups- elderly and young children w/ poor personal hygeine

sebaceous gland opening (skin opening)

hair follicle

wound/cut

minor lesions self resolve-keeping area clean

surgical incision and drainage

chemotherapy-topical antibiotics-oral antibiotics ineffective

can happen with staph aureus

higher risk in diabetics

young children usually

staph auerus subcutaneous infection

exfolitan or epidermolytic toxin

separates epidermal layer from derms-blistering and peeling of skin-exposes red under layer

general appearance of burned skin

syndrome begins as an erythema around the mouth and nose

spreads rapidly to infect skin of neck, trunk, and extremities

risk group with infants and young children ; 4 years (neonatal infection)

primary infected sites include umbilical cord and eyes-low mortality rate

death can occur as secondary infection of the denuded skin by other bacterial pathogens

tx-topical antibiotic mupirocin

infection from cellulose based tampons

had toxic shock syndrome toxin-1 (TSST-1)

death 2-5% from respiratory failure

can be prevented by removal of cellulose based superabsrobent tampons from market in 1980 CDC recomends that tampons are not used continously during a menstrual cycle

absorb and make low MG++ levels

inc growth bacteria of staphylcoccus aureus

triggers TSST-1 which is absorbed into the blood stream

TSST-1 (super antigen) stimulates T lymphocytes to produce cytokines intravenously resulting in endothelial cell damage-shock and multisystem failure

inital symptoms of high fever, vomitting, diarrhea and muscle cramps (myalgia)

ten days later-hands and soles of feet develop sun burn like rash which means peeling of skin, all over body and even tongue

severe sx-shock and multi-organ system failure

enterotoxin heat stable-not inactivated by digestive enzymes

toxin production does not alter food taste or smell

disrupts gastrointestinal lining

sx start in 4-6 hours

vomiting,cramps, diareehea, nausea

self-limited 24-48

dangerous because the microbes are carried to all body sites

bacteria reach site via

-focus of infection

-extensive surgery

-traumatic injuries

osteomyelitis (inflammation of bone)

pnemonia

endocarditis (inflammation of the endocardium)

meningitis (inflammation of the membrane surrounding the brain and spinal column

pyoarthritis-bacterial infection of joints

prolonged combination antibiotic therapy

drug regiment of 1 antibiotic, then another, then another, dec possibility of drug resistant strains

do not form virulent clot

staphylococcus epidermidis

staphlococcus saprophyticus

normal flora

common inhabitiant

human skin, respiratory tract and mucous membranes

Staphylcoccus epidermidis

staphylcoccus saprophyticus

normal flora

common inhabitant human skin respiratory tract and mucous membrane

Iatrogenic infection

infections related to surgical procedures that involve the insertion of foreign bodies, artificial valves, catherters (UTIS), prothetic hips and AV shunts (endocarditis)

opprotunistic infection

attachment of bacteria to foreign body

multiplication/colonization

types of infections include: endocardities, UTIS and wound infections

part of normal flora

common inhabitant lower intestinal tract and vagina

UTI, dysuria (pain in urination), pyuria (pus in urine), and high numbers of bacteria in the urine (should have zero in healthy urine)

2nd cause of UTI infections in sexually active young adolescent women

bacterial sensitivity or resistance to antibiotic novobiocin

staph epidermidis-sensitive

staph saphtophyticus-resistant

no vaccine is available

minimize opprotunity for infection

hygeine (hand washing)

adequate cleansing of wounds; change bandages frequently

attention to indwelling devices (catheters and needles)

tx surfaces w/ disinfectants

clinical presentation of px

isolation and demonstration of bacterium from clinical specimans (skin scrapings, blood, pus)

a. gram stain

b.innoculation of media

blood agar-enriched media with hemolytic pattern and colony color,

mannitol salt agar, selective medium (additive 7.5% NaCl), differential medium (fermentation of mannitol; monitor change in pH)

biochemical tests such as catalase tests and coagulase tests

neonates and surgical px

secondary transmission from "carriers" in hospital

carrier rate of staph aureus in general population is 30%

carrier rate of staph auerues in hospital pop is 70-80%

emerging superbug is methicillin resistant staph aureus or multiple resistant (MRSA)

health care associated (hospitals, nursing homes, dialysis center)

increased risk factors is older adults, weakened immune system, burns, surgical wounds, hospital stays and 10 days, invasive devices such as dialysis (catherterized) or feeding tubes, livnig in a long term facilitym recent antibiotic use

community associated MRSA

inc risk factors

daycare settings, NFL/NBA players, dorm residents, prisons, military training camps, gay men

crowding

frequent skin to skin Contact

Compromised skin

Contaminated items

lack of Cleanliness

tx is vancomyocin w/ combo

Gram positive bacteria

oval/spherical in shape (cocci)

grow in pairs or chains

**catalase-negative (staphylococci are catalase +)

2h2o2 (catalse enzyme)>2H2O+O2

fastidious-require complex media for growth in lab (perferably containing blood)

most are faculative anarobes (grows both aerobically and anaerobically)

large heterogenous group of bacteria-includes 100 diverse species that can colonize skin and mucousal membranes (oral cavity, nasopharynx, upper Respiratory tract, GI tract, genitourinary tract)

some memebres are harmless commensals, some are involved in food production (ex swiss cheese) others are impressive human pathogens

about 35 species have been identified aas sources of invasive disease in humans (ranging from local to systemic infections)

the most common human streptococcal pathogens, listed in order of prevalence and mortality are

1. S pneumoniae

2. S. pyogenes-group A Streptococcus (GAS)

3. S. agalacticide-group B Streptococcus (GBS)

4. Viridans streptococci (ex S. mutans)
pathogenecity is definied as the degree of damage caused by both the microorganism itself and the response of the immune system to the pathogen

attempts have been made to clinically identify strep by several class systems including

1. Lancefield group-serologic system based on reaction ofo specific antisera w/ surgace carb antigens

2.hemolytic pattern (RBC lysis) on blood agar plates (alpha, beta, gamma)

3. phenotypic traits (incl biochemical reactions w. antibiotic sensitivity)

4. molecular studies designating species and sub species

historically the classification of streptococci was based on the system developed by Rebecca Lancefield (1895-1981)

Strep strains were grouped according to the Carb composition on the cell wall antigens (but a strep can be pathogenic w/o one of these pathogens-just not lancefield patho)

there are 20 serotypes described as lancefield groupsA to V (exluding I and J) some strains are classified as "non Lancefield streptococci"

drawbacks to this approach include that the group-specific antigens may be absent b/w related strains or shared b/w distinct species

S. pyogenes: Grp A Strep "GAS"

infections are pharyngitis, skin/ soft tissue infectiosn

S. agalactiae; Grp B strep "GBS"

infections are neonatal pneumonia, sepsis

S. mutans, mitis, salivarius, thermophilus, sanguinis

Infections; caries, endocarditis

S. pneumoniae

infections: pneumonia, meningitis, otitis media (middle ear infection), sepsis

give plate an army green hue

differentiate b/w species w/ optochin test

sensitive to optichin (has zone of inhibition)-S. pnemoniae

no zone of inhibition/no optochin sensitivity-viridans streptococci (ex. S. mutans)

leave clear or yellowish area on plate (from agar)

differniate b/w species by evaluating suceptibility to antibiotic bacitracin

zone of inhibition w/ bacitracin-S. pyogenes (group A strep) (GAS)

no zone of inhibition-bacitracin resistant-S. agalactiae (group b strep) (GBS)

no hemolyiss

lancefield antigen group d most important w/in gamma hemolytic strep

molecular methods have determined the most sig gamma hemolytic group d pathogens belong to a distinct genus, Enterococci

group D non enterococcal strep (same habitat, ex GI and GU tracts) can cause endocarditis, UTIs, and are assoc w/ colon cancers- S bovis subspecies group

(16s RNA) designate 6 groupings

  ***See chart in strep lecture**

1. alpha hemolytic
2. optochin sensitive
3. not lancefield classified but still pathogenic
4. sig global cause of illness and death-particularly amoung children and elderly; responsible for 1.6 million deaths a year in children under 5
5. commonly colonizes in human nasopharynx esp of children-disease is rare (90% of children colonized by age 5; up to 40% of adults-prescence doesnt mean dx state)

• at beginning of 20th century, killed more ppl worldwide than any other bacterial pathogen
• today is most common bacterial cause of acute respiratory infections (sinusitis, pneumonia, and otitis media (middle ear infections))
• intermitent inhabitant of healthy human nose and throat (nasopharnx)
• transmitted person to person via respiratory droplets
• colonization does not usually rseult in dx however strains are typically carried asymptomatically for weeks to months
• however devastating consequences may result when organism gains access to lung, blood, or CSF

many cell molecules play a role in pneumococcal pathogenesis and virulence

2 promininent virulence factors

1. pneumolysin-secreted cytotoxin that lysis cells and damages tissues

2. polysaccharide capsule

***most important determinant of virulence-non encapsulated strains=no invasive dx

greater than 95 capsular serogroups identified to date-serotyping system is based on antibody reactions to capsular antigens, known as quelling reaction

13 serogroups responsible for majority of human dx

protects against phagocytosis

basis of pneumoccocal vaccines

clinical dx depends on site of infection and severity of infection and are classified as

1.non invasive-otitis media, sinusitis, non bacteremic pneumonia-in lungs, not blood stream

OR
2.invasive-bactermic pneumonia, meningitis, in lungs AND blood stream

**most common pneumococcal infection

primarily affects young children

usually follows a viral URI

sx-acute onset severe pain, fever, loss of hearing, swollen red and bulgin tympanic membrane

complication of URIS

often presents w/ facial pain, congestion, fever, and a persistent nightime cough

follows an infection of a normally sterile body fluid (ex blood, CSF), and can be life threateneing

include pneumonia, meningitis, and other invasive syndromes

most common serious pneumonoccocal disease***

diag by gram staining and culture of sputum-gram pos cocci

considered invasive when blood cultures are also positive

s. pneumoniae and neisseria meningitis are the most common causes of meningitis in children and adults

20% mortality even w/ antibiotic therapy

50% of survivors have permanent complications including deafness, mental retardation, personality changes, seizures

optimally: collect body fluid from site of infection by sterile technique

in case of non invasive dx, presumptive tx is often initatied after meeting diagnositc criteria

examine fluids by gram staining, culture, capsular antigen assay, and or PCR

tx w/ approp anitbioitics and dosages dependent of type and severity of disease

2 vaccines avail in US

1. PCV-13-developed specifically for infants and yound children, includes 13 capsular serogroups that caused most invasive dx and had most antibiotic resistance in this age froup

resulted in more than 90% dec in vaccine serogroup invasive dx

however-resulted in inc colonization w/ (and disease due to) other serogroup expressing strains

2.PPV-23 recommened for ppl over 65 years old and those 2-64 w/ underlying medical conditions

not as protective as PCV-13, lasts only about 5 years

relatively effective against invasive pneumoccocal dx

improved pneumoccocal vaccine formulations needed for adults

prevention and/or control of illnesses that predispose to pnemoccocal dx including flu vaccine, management of diabetes, heart and lung dx, HIV

reduction of antibiotic misuse-resistance prepetuates organism transmission and dx in the community

only species in Lancefield's group A (GAS)

Beta hemolytic

bacitracin sensitive

cause a variety of important human dx ranging from mild superficial skin infections to life threatening systemic diseases (est 700 million infections occur worldwide each year, although the overall GAS infection mortality rate is .1%;650,000 of the cases are severe and invasive w/ a mortality rate of 25%) *dont memorize this exact number in stats

infections typically begin in the throat or skin

colonization is infrequent and GAS is often pathogenic when present-if its there, you have it

can cause both pyogenic/suppurative (assoc w/ local bacterial mult and pus formation) and non pyogenic/non supportive syndromes (past infections/autoimmune syndromes)

produce a large # of products that contribute to the organisms pathogenesis

together the panel of GAS virulence factors allow the organism to attach to host tissues, evade the immune response, and spread by penetrating the host tissue layers

1. M Protein-major protein coating the cell surface, greater than 100 antigenically distinct types, contributes to resistance to phagocytic killing

2.hyaluronic acid capsule-not produced by all strains, protects against phagocytosis, weak immunogen (similar to hyaluronic acid on connective tissues), considered weak because we already have host antigens that are similar, immune response means autoimmune disease

3. many extracellular products including cell membrane damaging toxins streptolysins S and O (cause Beta hemolysis phenotype), streptococcal pyrogenic exotoxins (SPEs) A, B, C are linked to rash and severe invasive infections, proteins that enzymatically inactivate critical components of the host immune response (ex C5a peptidase, ScpC, streptodornase)

s pyogenes infections span the spectrum from mild to life threatening

non invasive GAS infections tend to be less severe and more commmon, these usually are effectively treatred with antibiotics

invasive GAS infections tend to be more severe and less common, these ocur when S pyogenes infects normally sterile areas (ex blood and organs), all severe GAS infections may lead to shock, multiorgan failure, death

spread by person to person contact

pharyngitis

affects all ages but one of the most common bacterial childhood infections

typically resolves in 3-5 days, tx given primarily to prevent spead and complications

has suppurative complications and non suppartive complications

result from spread of organism from the throat mucose to other tissues and the bloodstream

inlcludes; sinusitis, endocarditis, otitis media, bactermia, pneumonia, meningitis

autoimmune complications that can appear several weeks after initial strep infection and can include

acute rheumatic fever (characterized by inflammation of the joints and heat following strep throat)

and acute post infectious glomerulonephritis inflammation of the kidney (renal glomerulus) following throat or skin infection

less common non invasive strep A infection involving strep throat (usually) accomp by a characteritic "sandpaper" body rash and "strawberry tongue"

caused by release of SPES-streptoccocal pyogenic exotoxins

can cause a variety of infections of the skin, subcutaneous tissues, muscles, and fascia

impetigo-localized skin infect preventable by adequate hygeine, colonization of skin precedes infections, scratch, insect bite, tattoo etc inoculates organims into the skin

erysipelas and cellulitis is a mult and lateral spread of s pyogenes onto and into deeper layers of skin and subcutaneous tissues (fat=cellulitis), involves a skin rash infection of the upper layers of the skin which becomes bright red, tender, and raised (orange peel texture)

rare-bacteria invade and mult in the deeper layer of the skin, subcutaneous tissue and fascia

s pyogenes cause about 60%

usually begins @ site of trauma through which organisms are introduced into deeper tissue, usually from organisms residing on skin ex following minor trauma but can also originate from the bowel ex following abdominal surgery

severe dx of sudden onset, rapid progression, and requiring aggressive tx w/ surgical debridement and IV antibiotics

mortality rates about 75% if left untreated

presence of bacteria in blood

GAS bacteremia usually assoc w/ local infection (ex throat, skin, pneumonia, NF)

occasionally infectious complication of childbirth "puerperal sepsis"-once most common cause of maternal mortality

primary mech of bacterial spread to internal organs "hematogenous dissemination" can result in endocarditis or meningitis

streptococcal toxic shock syndrome

typically presents in ppl w/ preexisiting GAS skin infections that have developed bactermia

caused by release of SPEs into bloodstream

sudden onset of high fever, dec blood pressure, malaise, confusion, and rapid progression into coma and mult organ failure

mortality greater than 30% early recog critical for px to recevie aggressive medical intervention and antiobiotic therapy

no vaccine against GAS is currently avail

once GAS is documented as the cause of infection, antibiotic tx should be started promptly, dec incidence of invasive dx and both rheumatic fever glomeronephritis

for necrotizing fascitis, surgery is often also needed to remove damaged tissue and stop spread of infection

s. pyogenes infections are best prevented through effective hygeine (hand washing)

beta hemolytic

bacitracin resistant

belong to lancefields group B strep GBS

major cause of sepsis and meningitis in human newborns

cause of dx in healthy adult women related to pregnancy and childbirth

cause of invasive infections in adults with underlying chronic illnesses

GBS strains that cause human disease express a capsular polysaccharide (there are 10 serogroups)

GBS capsule is most important virulence factor

anti capsular antibodies protect only against GBS w/ the same capsule type (serogroup specific) (type 1-only against type 1 in the future)

occur w/in first week of life, 50% have infection signs at birth

infections occur during deliver from colonized in maternal genital tract (up to 40% of women are naturally colonized with GBS)

50% of infants born to colonized mothers also becomes colonized-1 to 2 % actually develop infection

infection presents as neonatal sepsis with respiratory distress-100% infants bacterimic, 50% have pneumonia, 33% have meningitis

occurs in infants 1 week to 3 months old

organism aquired during delivery or during later with colonized mother or hospital personale

meningitis most common presentation

infants may also have fever, seizures, bactermia, ostermylitis

majority of adult GBS infections in otherwise healthy adults related to pregnancy and childbirth-peripartum fever may involve endometritis, bactermia, meningitis, endocarditis

infections in other adults (non pregnancy related) involve the elderly or those with chronic illnesses (ex diabetes, cancer) often develops cellulitis, soft tissue infections ( diabetic skin ulcers), UTIS, pneumonia, septic arthritis, endocarditis

In US all preg women colonized w/ GBS tx'd prophylacticaly w/ antibiotics during delivery, women are screened by culture at 35-37 weeks of pregnancy, women w/ other risk factors also tx'd in absence of culture data (preterm delivery, prolonged labor, fever during delivery)

GBS vaccine in early stages but not yet avail, transplacental passage of maternal antibodies is protective for newborns, phase 1 trials of capsular vaccines suggest safe progess is being made

large groups of commensals, typically alpha hemolytic, some non hemolytic

differentiated from s pneumoniae based on optochin resistance and lack of polysaccharide capsule

lack lansfield antigens

predominantly inhabit the mouth

important agent in dental carries and endocarditis

perfingens-cause gangree, food poisoning

difficile-causes ulcerative colitis

tetani-tetanus

botulium-botulism

gram postiive bacili

spore formers-spores  eaten or contaminate injured skin

most are obligate anaerobes

most are motile

thioglycollate broth-anarobic growth (bottom of the tube)

litmus milk (curd formation)-stormy fermentation-plug, blows cotton out from gas production

blood agar-double zone of hemolysis-complete around initial colony then partial lysis

egg yolk agar-Beta lecithinase/a-toxin-turns plate white color, these degrade lecithin

histotoxic clostridia-C. perfingens

enterotoxic clostridia-C. perfingens and C. difficile

Cloistridum tetani

Clostridium botulinum

causitive agent is C. perfingens type A (spores found in soil)

opprotunistic pathogens that require a special enviro to initiate growth

traumitized tissue-lasceration, crush wound etc

vascular damage-impaired blood supply

necrotic tissue-dead, not receiving oxygen (anaroebic bacteria)

decreased oxygen

collagenase

proteinase

deoxyribonuclease

most advantagous***a toxin-phospholipase C-lecithinase-disrupts membrane of host cell

Theta toxin-hemolysin-lyses RBC's

A. anaerobic myonecrosis-gas grangrene ***more sever

B. Anaerobic cellulitis

infection of dead tissue, expands to healthy, ever widening of expansion of necrotic lesion adjacent to healthy muscle tissue

sx are local edema, action of a toxin-destruction of cell membranes

gas production-H2 and CO2-ferment carbs

change of skin color to black from dec blood supply

generalized fever

pain in infected tissue

example of this is road kill

traumatic injuries-wars, car injuries

surgical procedures in close proximity to intestinal microflora, bowel surgery, abortions

elderly-poor circulation

no host defense

phagocytic cells useless

repeated infections do not produce immunity

removal/debridement of dead tissue

application of antiserum (polyvalent antitoxin)

broad spectrum antibiotic-penicillin or tetracylcine

hyperbaric O2 chamber (inc O2 level)

localized infection of necrotic muscle tissue only-does not spread to healthy tissue

sx-similar to anaerobic myonecrosis but of a lesser severity

food poisoining

causitive agent C perfringens type A

second most common food poisioning worldwide

ingestion of viable vegetative cells

synthesis of enterotoxin in SI

enterotoxin produced which breaks down intestinal mucosa-leakage of plasma membrane-disruption of osmotic equilibrium

spores in foods, germination, ingest cells, positive enterotoxin in SI, disrupts osmotic equilibrium

watery diareha, abdominal cramps

no immunity, repeat attacks

cook food thouroughly intially-destroys spores

food refrigeration after prepartation-prevents enterotoxin production

reheating food-destrots toxin

spores-121 deg C

bacteria-100 deg C

toxins 80 deg C

antibiotic therapy

colonization of intestine by C difficile

toxins produced-injure intestinal lining by inhibiting protein synthesis, produces hemorhaggic necrosis

leukocyte infiltration into colon due to toxin production

pseudomembrane-white patch on colon-micture of fibrin, mucous, leukocytes and necrotic epithelial cells (due to inhibition of protein by toxin)

sx are abdominal pain, watery diareha, nausea,

risk groups are px receiving antibiotic therapy, primarily a dx of antibiotic induced colitis in hospitalized px

tx is discontinue antibiotics, maintain fluid, electrolyte balance, admin vancomyocin

generalized tetanus-initial involvement of neck and jaw muscles with progression to large muscle groups

neonatal tetanus-inital infection of umbilical stump, progression to generalized tetanus

favor spore germination

small puncture wounds

necrotic tissue at wound site

decreased O2

poly microbic infection-strict anaerobe, grows w/ faculative anaerobe dec level at that site, inc its ability to infect

neurotoxin-tetanospasm or spasmogenic toxin-toxin of primary importance accounts for classic sx

site of action-targets neurons in the spinal column

function is to bind to gangliosides in the neural tissue-blocks release of neuroinhibitor glycine-continual contraction of muscles (tetany)

neural tissue plus glycine (neuroinhibitor)-prevents muscle contration; when tetanospasmin blocks glycine-continual contraction occurs

initial-cramping and twitching of muscle around wound

later-sweating, pain around wound area, lockjaw or trismus-clenching of the law, muscle stiffeness neck and jaw muscles, risus sardonicus, sarcastic grin, opthotonos, arching of the back, want to keep external stimuli to minimum

extreme sx-preogression to other muscle groups, violents spasms of trunk and back-bone fractures

death can occur by paralysis of respiratory muscles

debridement of necrotic tissue

anti-toxin (only with free toxin-once bound-nothing to be done)

unimmunized-heman tetanus immune globulin (TIGH)-passive immunization

immunized-receive DPT series, may require a booster shor of tetanus toxoid**worlds most preventable disease

antibiotics-metronidazole or penicillin

anti-spasmic drugs or muscle relaxants-phenobarbital or chlorpromazine

neurotoxins A, B, E, and F-human dx

Neurotoxin A-(neurotoxin-hemagglutinin)

func of hemagglutinin-prevents deactivation of neurtotoxin by gastric enzymes and lowered pH of stomach

food borne botulism

infant botulism

wound botulism

mode of infection by ingestionof poorly preserved food containing Botulinin (botulinum toxin)

spores not killed

improper preservation created ideal enviro for spores to germinate

-anaerobic enviro, storage at room temp, alkaline foods (peaches, pears, more so than acidic tomatoes)

botulinin (botulinum toxin) product of metabolism

**most potent toxin-lethal dose 1 micro gram

toxin absorbed in GI, lymphatics and circulation, binds irreverisbly to NMJ of skeletal muscle (toxic site of action)

early-GI disturbane

NM sx-first affect muscles of head-same as C tentani, blurred speech and double vision (diplopia), slurred speech (dipphonia), difficulty swallowing (dysphagia)

critical sx-descending paralysis w/ involvement of respiratory system fatal for 8% infected

cov/immunity-repeated infectionsdo not produce immunity, small amount of toxin in the circ, toxins have strong affinity for neural tissue

tx-polyvalent antitoxin therapy, stomach lavage and enemas

control/prevention-adequate food prevention-kill spores, heat all canned food, toxin inactivated at 80 deg C for 20 min

assoc w/ SIDS

flaccid paralysis of floppy head baby syndrome

ingestion of spores, dietary supplement honey, multiplies in colon due to immature state of neonatal intestine and flora

indicators-suck and gag reflex dec, drooling, head control lost

tx, antibiotic tx

contol prevention-vaccinate preg females-passive immunity mother to child

rare neuroparalytic disease

spores enter a puncture wound-in vitro toxin produced

sx similar to food borne botulism

risk group is IV drug abusers

family of bacteria that primarily reside as normal flora on mucosal surfaces

most sig human pathogens of this genus are Neisseria meningitis, a cause of septicemia and meningitis and neisseria gonorrhoeae

N. lactamica

N. cinerea

N. polysaccharea

N flava

N subflava

N mucosa

N flavescens

N sicca

gram neg diplococci

fastidious growth requirements-grow optimally at 37 deg C in 5% CO2, require highly enriched media

fragile, do not survive well in hostile growth conditions, cold/hot temps, UV lights, dry/arid conditions

N meningitidis may be transient to normal flora-can have in back of throat and be perfectly healthy whereas prescnene of N gonorrhoeae is pathogenic/disease state

N meningitis infections: low prevalence but high mortality whereas N gonorrhoaeae infections high prevalence byt low mortality

1.  Humans are the only natural host

2. colonize the URI

3. Transmitted via large droplets respiratory secretions

-10% healthy adult humans are colonized

-despite exposure/colonization few develop dx

4.life threatening cause of meningitis and sepsis

5.produce a capsule the primary virulence factor****

Capsule is major virulence factor

undergo phase (ON/OFF) and antigenic (type/variety) variation

exhibit "molecular mimicry"-mimic human antigens-make it harder when mimics host

large struc polysacch layer surrounding the outside of the bacterial cell

protects against host immune factors and desiccation

important for invassive diseases

used to group N meningitis into 13 serogroups

serogroups A, B, X, Y, and W135 are the most pathogenic

may be immunogenic and elicit protective antibodies

caused by infection with N. Meningitis

results in a high mortality rate, even w/ tx

cause of life threatneing men and sepsis (blood infection)

meningitis: bacterial infection of meninges, the membranes that surround the brain and spinal cord

meningococcemia: bacterial infection of the blood/ other body organs, form of septicimia

men and meningococcemia are major causes of illness , death, and disability

spread from person to person via direct contact with respiratory secretions, saliva, sputum or nasal mucus

requires close contact with an infected person/carrier including: kissing, sharing items that touch the mouth (drinks/eating utensils/cigs/chapstick), being w/in 3-6 ft of an infected person who is coughing and sneezing

crowded living areas (dorms, baracks, prison)

not getting enough sleep (weakened immune system)

exposure to cig smoke (active or passive)

arid living conditions

alcohol use

viral URI

travel to endemic area (sub saharan africa and mecca)

compromised immune system-harder to fight off disease

1. 6 of 13 capsuel serogroups cause human disease: A, B, C, X, Y, W135

2. MC cause sporadic disease, community outbreaks, large epidemics, 250 to 500k cases per year worldwide (inc if epidemic occurs), epidemics occur every 8-14 years in the african meningitis belt, about 500 to 1000 cases per year in the US (since 2005)

3. high case fatality rate (even w/ microbial therapy), children b/w the ages of 6 months to 4 years are highly susceptable

4.meningococcal disease usually presents clincially as one of 3 syndromes: meningiits (50%), bactermia/meningococcemia (37.5%) or bactermic pneumonia-can cause pneumonia(9%)

5.leading cause of bacterial meningitis in young adults 19-27 years old

epidemic outbreaks (ex african meningitis belt), primarily caused by serotype A followed by W135, C, X

sporadic outbreaks, caused by serotypes B and C followed by Y, W135, A

disease rates peak winter through early spring (dec through june), constant irritation of respiratory mucosa from dry enviro and colds

10-50% of infected people die despite receiving antibiotic tx

survivors often have permanent probs: loss of limbs, deafness and or blindness, mental retardation, strokes, seizures, behavioral issues/personality changes

following aspiration of N meningitis, bacteria may be elminated or colonize the nasopharynx

colonized indiv may remain asymptomatic "carriers" or develop a mild/moderate sore throat, pneumonia may develop, human nasophar only reservoir for MC (obligate human path), colonizing commensal of 3-25% of pop globally, correlates to 230 mill-1bill carriers worldwide, path of MC resembles the story of jekyl and hyde

in some cases (less than 1%) the bacterai cross the mucosal barrier and enter the blood stream or CSF resulting in either

-mild disease-self limiting bactermic illnesses charac by fever and malaise sx resolve in 1-2 days

serious disease infection may progress to miningococcemia and/or meningoccocal meningitis

aka meningococcal septicemia

virulent N meningitidis invade into the bloodstream

sx are initially similar to fle infection including fever, nausea, headache, muscle/joint pain, chills, diareha, malaise

MC in the bloodstream results in an affre systemic response, small blood vessel damage results in small hemorrhages (petechiae), in severe infections further samage to blood vessesls can cause vascular collapse and large hemhorrages (purpura fulminans)

severe systemic infec charac by rapid circ collaspse and prog multi-organ failure

occurs in 5-15% of px w/ acute meningococcemia

abrupt onset of sx includes sudden appearance of widespread hemorrhagic skin lesions (hemorrhagic rash)

no signs of meningitis are typically presently-progressing so rapidly

very high concen of MC in the bloodstream

high mortalitiy (50%) w/in 12-24 hours of onset despite antibiotic therapy

most common outcome of MC disease

sx may include sudden onset of severe headache, high fever, malaise, chills, vomiting

progressive stiffness of the neck, back, and soldiers

neurologic issues are sensitivity to light (photophobia) and sound (phonophobia), altered mental status

convulsions, coma

petechaie or purpura may or may not be present

**rash is a big warning sign

10-25% of cases are fatal even w/ tx

survivors often have permanent damage seizures, deafness, MR, behavioral issues

when meningococcal disease is suspected, tx must be immediately started and not delayed for confirmatory lab tsets

gold stand of dx is isolation of N men bacteria or DNA from either blood or CSF samples (both are normally sterile), diag relying on culturing organsims on chocolate agar plate followed by further testing to differentiate the species takes about 24-28 hours

NAATS (nucleic acid amplification tests) such as polymerase chain reaction (PCR) based assesments are now often used to identify the organism w/in several hours from hospital admittance

grams stain CSF shows gram neg diplococci (often inside neutrophils) can confirm dx and support initiation of immediate therapy

beside immediately tx'ing px, confirming etiology as an MC infection is important for the prevention of secondary cases and epidemiology (serogroup, antibiotic resistant profiles)

potentially fatal medical emergency

prompt anitbiotic therpay is essential for survival

even with tx death or permanent disability often occur

preventative antibioitc tx, isolation, and or vaccination is necessary for close contacts of an infected person

majority of meningococcal disease in the us is caused by strains of producing capsular serogroups B;C;Y

Polysaccharide based meningococcal serogroup A, C, Y, and W135 vaccines are avail in US and have been recommended by the CDC for routine use snice 2005 for

-all adolescents aged 11-18; 1st dose at age 11-12 yrs, booster at 16-18, booster lasts 3-5 years

people 2 months-10 years old or greater than 19 if at high risk for mening disese, includes indiv w/ certain med conditions, (ex damaged/missing spleen, immune deficiencies), high risk living enviro, (dorms, barracks,) occupational exposure, travel to endemic area, control outbreaks if in close contact with dx case of MC disease

Serogroup B causes 30-50% MC cases

until recently there were no MC serogroup B vaccines liscened for general use in the US

b/w oct 2014 and jan 2015 the FDA approved 2 serogroup B MC vaccines (Trumemba, Bexaro) for use in US for people 10-25 years of age

these vaccines will be important tools for controlling outbreaks of serogroup B meningococcal disease

although there is no routine recommendation for serogroup B meningococcal vaccines at this time, 2015 is going to finalize these

humans are only natural hose (obligate pathogen to humans)

higher prevalence, lower mortality

aquired by sexual contact

caustive agent of STI gonorrhea

affects mucous membranes of urethra, cervix, rectum, pharynx, and conjunctiva

high transmission rate

may cause disseminated disease and permanent damage

essentialy same virulence factors as N menin (LOS, OMPS, pillis) but NO CAPSULE

one of the oldest known human diseases

major public health problem

750,000 cases/year in the US (;1/2 reported)

ranks 2nd amoung communicable diseases in the uS

majority of infections are asymptomatic and therefore not reported and tx'd

new infections are ususally contracted from an infected sex partner with no or minimal sx

attack rates highest in 15-29 yrs, inc in older pop since 98 (viagra), but occurs all ages

infection not protective

transmitted person to person through infectious secretions

after 1 of sex w/ infected parter 20-30% men infected, 50-90% of women infected

GC can be localized and systemic infections

untreated gonorrhea can cause serious and permanent damage and health probs in both men and women

acute urethritis (usually dev w/in 5 days), painful urination, purulent urethral discharge "the drip", localized inflammation (redness, swelling, heat, pain)

may be asymptomatic, asymptomatic males are important reservoir for transmission and are at inc risk for developing complications

untreated gonococcal infection: may resolve on its own, but most likley not before it is transmitted to a partner, GC may invade the prostate or testicles and cause infertility and/or become systemic

primary site of infection is cervix, but bacteria can be found in the vagina, urethra, and rectum

sx are often mild and non specific

more than 50% infected women are asymptomatic and receive no tx

inc risk of infecting a partner

severe health consequences if untreated-can progress to uterusm fallopian tube, ovaries; PID may develop, increased risk disseminated infection

generic term inflammation of uterus, fallopian tube, and or ovaries that leads to scar formation on nearby tissues and organs

bacteria ascend the reproductive tract infecting and causing inflammation of the uterus, f tubes, ovaries and destroy mucosa

PID scarring often causes permanent damage, ectopic preg and other dangerous complications, severe or chronic ab or pelvic pain

infertility-PID can be directly responsible for infertility, 12-20% of women become sterile after 1 episode

aka DGI

conococcemia or arthitis-dermatosis syndrome

condition charac by hemorhaggic pustles, rash, recurrent fever, body aches, pain/and or arthritis in one or several joints

affects 1 to 3 % untreated GC px

bacteria cross mucosal barrier and enter bloodstream

results in bactermia and systemic dx

blood cultures are pos

endocariditis and men may develop (rare)

infants:aquire GC during delivery

1.opthamalic neonatrorum-gonococcal conjunctivitis is a major preventable cause of blindness in newborns, antibiotic eye drops given to prevent

2.DGI possible-may result in joint infections or a life threatening blood infection in the baby

Children: clinical infection of GC infection is dx for sexual assalt/abuse

laboratory charac

1.gram stain-used for presumptive ID of GC infections in urethral and cervicalexudates, must be confirmed, not recomended for pharyngeal or rectal specimans

2. culture-clinical specimans cultured on selective media (thayer-martin), culture blood/CSF if DGI suspected

3. presumptive dx of GC infections depends on, typical colony morphology, gram stain, postive biochem tests

additioanl tests must be performed but antibiotic therapy can start w/o

nucleic acid amplification tests (NAATs) detect pathogen specific DNA or RNA in a clincial speciman

developed in response to difficulties in maintaining approp culture conditions

do not require viable bacteria-are specific, sensitive, and reliable

antibiotic therapy is effective in elim the infection

inc prevalence of antibiotic resistant strains-an emerging public health threat

asymptomatic infections=no tx=inc risk for comp and transmission

antibiotic therapy will not repair permanent damage-ex like infertility issues

prevention of GC infections:

1.no effective vaccine currently avail to prevent gonorrhea

2.infection is not protective against reinfection

3. to avoid/dec risks of GC infection, practice abstinence/safe sex, seek prompt medical attention for abdominal urogential sx, inform all recent sex partneers if dx so they can seek tx

***asymptomatic males and females major problem

gram positive rod

more frequently seen in immunocompromised px, high freq of disseminated infections in pregnancy

seen in neonates, elderly, and imunocompromised

freq causes infections in CNS

exhibits tumbiling motility (tumbles around in drop of saline) from flagella

can be mistaken for gram neg when discolorized from improper technique

requires thourough pasterization

can multiple at 4 deg C-ex in grocers fridge

zoonois

assoc w/ milk and milk products in particular soft cheeses

any failure in pasteurization can lead to organisms that then mult at 4 deg C or survive in freeze

2000 cases/yr and around 400 deaths/year

happens freq in infants younger than 1 month, adults older than 60, pregn women, alterred cell mediated immunity

ingestion of organisms

replicates intracellularly: like S typhi, tuberculosis, legionella penomphila

attaches to intestinal epithelial cell and macrophages

once in phagolysosomes secretes a hemolysin (listeriolysin) which allows escape from the phagosome and pelication in the cytoplasm

alter cell shape and actin extreded processes aloow for cell to cell spread

predilection for the placental and CNS

large outbreaks generally dairy products, recently cantelopes and caramel apples

innate and cellular immunity

preg and neonate have lowwered immunity

lymphoma, transplant px on imminosuppressive, AIDS px, px on steroids, other cell mediated immune defects

px receiving TNF blocking agents

elderly

pregnancy and neonates-women infect placenta and fetus in utero-"vertical transmission"

meningitis and encephalitis, bacteremia-in AIDS px, elderly, transplant px

ampicillin-penicillin base works and inhibits peptidoglycan

trimethorim sulfamethoxasole

--said we wont really have to know this slide

thoroughly cook raw food from animal sources

wash raw veggies and fruit througholy before eating

keep uncooked meat sep from vegs or ready to eat food

avoid unpasteurized products from unpasteurized milk

wash hands, knives, and cutting boards after handling uncooked foods

comsume perishable and ready to eat foods asap

dont eat uncooked meat

pay extra attention to avoid dairy, soft cheeses, european food often not pasteurized, packaged meat, fishes

other types corynebacterium part of normal flora

dipthera comes from greek word leather

gram pos bacillus-"chinese letter appearance"

grows on blood agar but use of tellurite agar improves ID and recovery

dx producing strains carry a beta phage encoding gene for toxic production (tox+)

previoulsy devastating dx w/ epidemics now controlled largely through use of vaccination

humans now only reservoir

spread by droplet or airborne spread

went from 200,000 cases/yr to about 5

young children seem to be proteced mothers antigens

may be possible lack of follow up immunizations b/c this

The 2006 WHO summary

-8229 cases of dip worldwide

78% were from SE asia with 89% of those from india, greater than 30 cases from afghanistan, haiti, DR, indonesia, papua new guinea, phillipines, vitenam, nigeria

non invasive (localized infection=non invasive)

extoxin is produced:

-2 segments: B which binds to spec receptors on susceptible cells, and A, the active segment

**toxin ADP-ribosylates Elongation Factor (EF2) which is responsible for translocating tRNA resulting in cessation of protein synth(also seen w/ cholera and pertussis toxin)

targets heart (myocarditis), nerves (demylenation), and kidneys (tubular necrosis)
VERY POTENT TOXIN**

pharyngeal infection causes local necrosis and formation of pseudomembrane

this membrane is a leathery collection of cells attached to back of throat

this can detach and cause asipiration/suffication

bull neck assoc w/ massive lymphadenopathy

related to extent of local dx and toxin production

cardiac-can be acute disease w/ CHF, myocarditis, conduction disturbances or a more chronic presentation

neuropathy both peripheral and cranial nerve neuropathy

renal

no natural immunity

toxoid vaccine-formalin-inactived toxin used as vaccine

3 in the initial series, prior to high school, then every 10 years w/ Td

tx-penicillin and erythromicin should be active

may need antitoxin in severe disease

biblical references to inflames papules

first disease attributed to a bacterium by Robert Koch in 1877 and fulfilled what became known as kochs postulates

pasteur developed attenuated strain and animal vaccine

inhalational anthrax among 19th cen british and german woolsorters and rag pickers

"accidental release of anthrax spores" 1979 from USSR facility in russia-70 cases

22 cases of human anthrax and 5 deaths-relatively lethal

gram pos bacilli, non hemolytic growth on blood agar

***sporulates in prescence of O2

bacilli w/ prominent centeral or paracentral oval spores that do not cause swelling of the bacilli

poly-d-y-glutamic acid (PGA) capsule important in inhibition of phagocytosis of vegetative bacilli

catalase pos

non motile

"boxcar shape" oblong w/ central spore

PGA capsule encoded on the pXo2 plasmid

pXo1 plasmid encodes 3 components: protective antigen (PA), edema factor (EF), and lethal factor (LF)

Edema toxin-composed of PA combined with EF, produces local skin edema

lethal toxin-composed of same PA together with LF, was highly lethal for experimental animals

Combo of all 2 most lethal and produced many charac of actual anthrax infection

PA-so called b/c as an Ag it produces protective antibody, cleaved by cellular proteases to form heptamer

when the PA  heptamer complexes w/ EF, it forms edema toxin, EF is a calmodulin-dependent, adenylate cyclase that inc intracellular cAMP concen and interefers w/ cell func

when the PA complexed w/ LF it forms lethal toxin, LF is a zince metalloprotease that cleaves and inactivers mult mitogen activated protein kinases (MAP kinase) and interfers w/ signal transduction

toxins are then taken into cytosol where they mediate cellular damage

2 component toxin-active site is actual toxin

local inoculation of spores

no purulence and painless

development of classic black eschar (scab); from dec blood supply

dev of significant local dx

woolsorters dx-wool serpartaing put spores in air

rapid dx progression

pleural fluid and widened mediastinum-enlarging and hemorrhagic medistinal nodes

rapid progression to death

most common dx assoc w/ anthrax contaminated mail

GI- ingestion of contaminated food, unusal in humans

CNS anthrax-Meningitis, rapid progression, 1st case in the US post 911 cases

ciprofloxacin-quinolone

penicillin

tetracycline

-later 2 may be less effective in bioterror cases if resistance has been engineered in

stomanch, duodenum, jejunum has 1.0 x 10^2 bacteria

proximal ileum is 1.0 x 10^3

distal ileum is 1.0 x 10^8

colon is 1.0 x 10^11

human body has 6.0 x 10^13 cells

total bacteria is 1.0 x 10^14 bacteria

from 60x to 100x more bacteria than eukaryotic cells in our body

Salmonella Spp

Shingella Spp

Yersine Spp

Vibrio Spp

Campylocbacter spp

helicobacter spp

escherichia coli

clostridium perfingens

bacillus spp

five prior "species' were reclassified as a single species: S.enterica with 5 major pathogenic serovars

Serovar is a group of closely related microorganisms distinguised by a charac sert of molecules that evoke and antibody response

S enterica Serovar tryphinmurium-mouse typhoid fever-can infect humans w/ mild GI

S enterica S coleraesuis-swine gastroenteritis

S enterica S enteriditis- gastroenteridis

S enterica S typhi-typhoid fever (human)-can be lethal

S enterica S paratyphi-Typhoid like (human)

gran neg

motile (Flagellated) bacillus

faculative anerobe

non lactose fermenter-utilizes other sugars

oxidase neg (reduction of DPD) (DPD=N,N dimethly-p-phenylenediamine)

sulfur reduction (alt energy production)

LPS: consists of O polysachh side chaine-lipopolysacch, in outer membrane, used for serotyping of strains

difficult to do a basic culture from a fecal matter test due to the large amount of bacteria in the GI

have to take advantage of phenotypes and growth requirements

salmonella is a non lactose fermenter and does sulfur reduction

use salmonella-shigar agar

selective medium for gram neg bacteria-bile salts inhibit Gm+

sugar utilization, colonies that ferment turn red due to an acid production that occurs during fermentation

sulfur reduction is from use of sodium disulfate in agar, if sulfur reduction occurs end product is black

flagallae-composed of arrays of flagellar proteins

very antigenically diverse in salmonella

antibodies against the flagellae of one strain of salmonella will not bind to flagellae expressed by a different strain of salmonella

have different side chains of LPS's in diff strains to create this diversity

over 2,000,000 cases annually in US

recent outbreak in peanut butter

oral entry of infection

usually limited to intestine (non disseminiated-remains in GI)

invasive bacterium-enters into cytoplasm of gut cells

fever, nausea, cramps, diarehea

diarreha-electrolyte imbalance, dehydration

self limiting disease (2-4 days)

rarely can be fatal

stim its own uptake into gut cells

induces rearrangement of the actin cytoskeleton of the host cell

plasma membrane "ruffling" observed prior to invasion by salmonella into the host cell

obligate human pathogen

oral uptake; invades via intestines

dissemination from intestine via macrophages to lyphatics, blood, liver, kidneys, gall bladder, etc-sytemic bactermia

reinvasion of intestinal epithelium (hemorrhagic ulceration) this is like a crack in the intestianl epithelium

chroninc (asymptomatic) carriage in the gall bladder; shedding into the intestine "typhoid mary"

goes to GI, then systemic, then back to GI

gut epithelium

peyer's patches-collections of m cells

m cells-set of specialized gut phagocytotic cells, uptake of proteins and other particles

salmonella spp exploit M cells for cellular invasion

salmonella invase the intestinal epithelial cells to initiate infection

uptake replication in a phagosome survives in the phagosomal compartment

salmonella remain w/in membrane bound phagosome when in cell cytoplasm

S. enteridits has a deep tissue invasion

S typhi continues on to have systemic circulation

mapping of virulence genes illustrated that the viruclence genes were clustered in the chromosome

pathogeniticy islands SPI-1 and SPI-2

know the genes in the section are important because mutations or deletions can reduce infective capacity causing avirulence

also found knocking out specific genes could cause complete loss of virulence because these genes had a special secretion system

injects proteins into cytoplasm of infected cell to manipulate cell functions (bacteria has to interact w/ cytoskeleton but this secretion system actually gets it inside)

comes from SPI-1 (pathogenesis island 1)

injects sip/ssp effector proteins into the cell

these proteins are actually injected like a hyperdermic needles

stimulates uptake of bacterium into the host cell

responsible for survival in host cell after path island one actually gets it inside

participates in avoidance of antimicrobial activities, modification of cellular trafficking, intracellular survival and replication

secretes SSE-salmonella secretion effector proteins

causitive agent bacterial dystentary

all 4 species cause bacteria dysentary

shingella boydii-uncommonly isolated

shingella flexneri-developing countries

shingella sonnei-industrialized countries

shingella dysenteriae-most severe infections, can be lethal

humans are only reservoir for shingella spp

obligate human pathogen

highly infectious (only 5-50 bacteria needed to elicit a shingella infection)

(salmonella need 100,000 to 1 million to cx infection)

about 24,000 causes in 1995 in US

gram negative, non motile bacillus (no flagellae)

faculative anaerobe (aerobic or anaerobic)

non lactose fermenter (utilizes other sugars)

oxidase neg

LPS-consits of O polysaccharide side chains-used for serotyping of strains

bile salts to inhibit Gm+ bacteria

lactorse, sucrose, salicin

bromothymol blue for sugar fermentors (acidic-yellow/fermenting)(alkaline-blue/green)

shingella produces raised, green, moist colonies

oligosaccharides of LPS are MUCH less diverse than in salmonella

only about 45 antigen serotypes

no flagellar antigens

abdominal cramps, fever, diareha which sheds bacteria

infections of submucosal cells of the lining of the intestine, does NOT commonly disseminate beyond the gut

inflammation, loss (sloughing) of the epithelial cells of the gut lining

ulcerative lesions form on lining of gut

stool contains copious amounts of mucous and blood-unlike salmonella infections

dehydration and elctrolyte imbalances can be LETHAL

pWR501

encodes genes for invastion

extrachromosomal invasive phenotype, 200 kbp

30,000 bp region of the plasmid=required for the invasive phenotypes

"entry region"-encodes invasion (Ipa) proteins and a type 3 secretion system

type 3 secretion system injects Ipa proteins into the cell

invades through M cells

invades epithelial cell in vacuole

type 3 secretion system injects Ipa into cell

lysis of vacuolar membrane (IpaB)

escape from phagosome and relase of the bacterium into the cytoplasm; rich intracellular "soup"

replication occurs in cytoplasm

shiga toxin interrupts ceullar protein synthesis

no flagellae-unique type of mobility controlled by IpaC

induces actin polymerizatin in the host cell for rocket propulsion for cell to cell spread

hides from the immune system w/in the infected epithelial cells

physically moves cell to cell

more than 2400 O serotypes (Ab specific)

more than 119 H (Flagellar) serotypes

viral, parasitic, bacterial, fungal

about 20 million a year

about 1 million people a day contract an STI

stis often have no warning signs or sx

complications can progress before infection identified

true incidence vastly underestimated

large proportion infections asymptomatic

15-24 represent only 25% of sexually active pop but account for about 50% of all STI dx/yr

est about 12000 24 year olds contract an STI every day in US

female 4 times more likely to contract

chlamydiae are gram neg obligatge intraceullular bacteria-depend on host cell for survival and replication

chlamydiae consist of 3 speicies-all cause human disease

c. trachomatis-causes ocular and genital infections

c. pneumoniae causes outbreaks of respirtatory tract infections, spreads from person to person

c psittaci-transmitted from infected birds or animals to humans through RT, causes in flu like illness called psittacosis

1.chalmydia (STI) and trachoma (eye dx) are caused by gram negative bacteria chlamydia trachomtis (chlamydia infection also refers to infection caused by any species belonging to genus chlamydia)

2.c trachmatis is naturally found living only inside human cells

3.one of the most common treatable STIs worldwide (>95 million cases/year)

4.single most important infectious agent assoc w/ blindness-approx 600 million worldwide suffer C. tachomatis eye infections and 20 mill are blinded as a result of the infection

can be transmitted vaginal, oral, anal sex, childbirth

**Most common STI in US-1.4 mill cases in 2013, est 3 mill assitional ppl are infected in the US w/o knowing due to asymptomatic

known as silent epidemic b/c in 75% of cases in women it may not cause any sx-of those who have an asx infection that is not detected, 50% will develop PID

PID can cause scarring inside the reproductive organs which cause serious complications, including chronic pelvic pain, infertility, ectopic (tubual preg)

affects all ages, most common 15-29

as many as 1 in 4 men have no sx

may produce sx similar to gonorehae which include burning during urination, discharge penis or rectum, testicular tenderness or pain, rectal pain

3 in 4 women experience no sx

burning during peeing, painful sex, vaginal discharge or bleeding after intercourse, rectal discharge or painl, abdominal or lower back pain, sx of pid, liver inflammation similar to hepatitis

untx'd infections can cause serious preoductive and other health probs w/ both short-term and long-term consequences

-PID (women) chlamydia causes quarter mill/half mill PID sx a year

sterility (men and women)

blindness (women and infants)

lymphogranuloma venerium-infection lymph nodes

reactive arthritis (reiter's syndrome)-triad of arthritis, conjunctivitis, and urethritis (inflammation urethra most common in men)

infants-maternal infect may result in spontaneous abortion, premature birth, conjucntiviis (possible blindness), and pneumonia, half of all infants born to mothers w/ chalmydia will be born with dx

NAATS prefered dx tool-specimens obtrained vaginal swab in women, first catch urine in men

approp antibiotic tx for chlam is crucial (has to penetrate into cell)

early antibiotic tx extrememly successful and may prevent the development of long term permanent complication

untx'd infection may result in infertility

follow up eval should be done after 4 weeks to determine cured state

can get mult stis from same encounter-pos for one means screened for others as well

other parters should be screened as well

all must be tx'd

no immunity following an infection

increases changes of HIV infection 5 fold

if preg can cause premature labor and delivery, in addition infact may develop chlam conjunctivis and pneumonia

safe sex-condoms

annual screening women sexually active 25 and younger, women over 25 with newer or mult sex partners

call dr if experiences sx

screening periodically

can't be contracted through toilets, daily activities, hot tobs, sharing utensils, clothing

previous infection not protective against reinfection

distinctive gram neg bacteria which are long, thin, motile, spiral cells

widespread in viscous enviros (aquatic sediments and mud, biofilms, mucosal surfaces) found in intestinal tracts and oral cavity of mammals

distinguised from other bacteria by location of flagella (aka axial filamanets) which run lenthwise b/w bacterial inner and outer membrane

when filaments rotate, move in cork screw fashion through enviro

dx causing members of phylum include

treponema palllidum-sphyillis

borrelia burgdoferi-lyme disease

borrelia recuurentis-relapsing fever

leptospira species-leptospirosis

sphyillus

bacteria spread through broken skin or mucous membranes, transmitted sexually and disseminates, can be passed in utero to cause still births, newborn death, defomities, seizures

can persist for decades in human host

challenging to study b/c can't be cultured or genetically manip in lab-must be propogated in rabbit testes to maintain strains for research investigations

several stages-sx depend on stages-many people do not have sx

can be generally tx'd w/ antibiotics, if left untx'd syphillus can damage heart, brain, eyes, and bones, in some cases this can be fatal

believved to have infected 12 million people worldwide w/ grater than 90% in developing world

rates cont to inc since turn of millenia

partially due to inc unsafes sex practices

currently widespread in US-affects sexually active adults ages 15-45 and esp gay dudes

can also be aquired with iv abuse

after being on verge of elim in 2000 in the US, syphillus cases have rebounded

75% of 1st deg and 2nd deg occured amound gay dudes

33%-50% of indiv become infected after sexual contact with syphillic partner

primary stage

painless small open sore called chancres form at infection site about 2-3 weeks after infection

heal and dissappear in 3-6 weeks, may go unoticed in rectum or cervix

enlarged lymph nodes may occur near area containing the chancre

bacteria continue to mult but there is little evidence of dx until 2nd stage

if untx'd will progress to 2nd stage

bacteria spread into bloodstream

occurs about 2-8 weeks (up to 6 months( after chancre forms)

most common sx is skin rash usually on palms and soles

lesions called mucous patches may be seen in mouth of gentials

moist, warty patches may develop on gentials or skin folds

additional sx like malaise, fever, general ill feeling, loss of appetite, muscle aches, joint pain, enlarged lymph nodes, hair loss may also occur

sx go away as bacteria becomes dormant again

final stage of syphillis-follows intial infection 3-15 years (up to 50 has been documented)

bacteria grow and spread to brain, CNS, heart, skin

pockets called gummas affect various tissues and are very destructive

sx depend on which organ system affects

"great imitator" because 1st and 2nd stages long forgotten

life threatening complications 3 deg syph rarely seen today b/c early detection and tx

late syph is premenatly disabling and may be fatal

cadiovascular syph-aneurysms or valve dx

neurosyph-CNS and neurologic disorders

gummas-destructive, infiltrative tumors of skin bones or liver

can be completely cured if dx early and tx'd thouroughly

1st and 2nd deg can be tx'd w/ antibioitcs

follow up blood tests must be done at 3,  6, 12 and 24 months

avoid sex when chancre present, uses condoms until 2 follow up tests neg

partners tx'd

can't be contracted toilets, hot tubs, clothing, utensils

no protection previous infection

gran neg spirochete that causes lyme dx

unlike t palidum, can be cultured in lab, however bacterium is fastidious and requires complex growth medium-even under optimal conditions

invades blood tissues infected mammals and birds

natural reservoir is white footed mouse

ticks transfer spirochetes to deer, humans, and other warm blooded animals after a blood meal on infected animal

named after lyme CT from outbreak in 1975

cause of tick borne dx remained a mystery until 1981 when identified, also has been around for a long time

classified as a zoonois

most common tick borne infectious dx in N. America and N hemisphere

3 interrelated elements must be present for lyme to exist in an area-

1.B. burgdorfeni bacteria

2. ticks that can transmit them

3. mammals to provide food

lyme disease occurs in stages

life cycle of B burgdoferi is complex requiring ticks, rodents and deer at various points; micre primary reservoir, ticks then transmist bacteria to other humans

most infections caused are by nymphomal stage ticks-small nymphs produce secretions that prevent the host from feeling any itch or pain from bite, as a result, the ticks may feed for long periods of time unprotected

transmission quite rare, takes more than 24 hours for attachment for bacteria to transfer, thus tick checks useful

can spread throughout body during course of dx, found in skin, heart, joint, PNS, CNS

as a result can affect mult body systems and produce a range of sx-many sx result

incubation period 1-2 days but can be hours or years

infection can be elim by antibiotics if illness dx early

delayed or inadequate tx can lead to more serious sx, which can be diabling and difficult to tx and persist for decades

early localized infection

circular expanding rash called eythema migrams (EM) that has bullseye appearance

also flu like sx such as headache, muscle soreness, fever, and malaise

can progress to later stages in px who do not develop a rash

early disseminated infection

can be dayts to week after local infection onset

may disseminate from tick bite

EM may develop at additional sites

other sx heart palpitation, dizzieness, and/or migrating pains in muscles, joints, tendons

various neuro sx included facial palsy, muscle/joint pain, shooting pains, abnormal skin sensations, sleep disturbances, mood changes/alterend mental status

late persistent infection

after several months, px may go on to develop severe, chronic, and disabling sx that affect many parts of the body including brain, nerves , eyes, joints, and heart

lyme arthritis, usually in knees or larger joint, in 10-15% may lead to erosion of cartilage or bone

chronic neuro sx in 5% px involving shooting pains, numbness, tingling in hands or feet, profound fatigue, difficulites concen or short term memory probs, neuropsych affects

lyme disease dx clinically based on sx, onjuective physical findings, hx or possible exposure to ticks, serologically blood tests (Not effective til later stages)

EM rash considered sufficient for dx even when blood tests neg, however not all px will get a charac rash or recall tick bite

bottelia are slow growing and can delay dx

dx late stage lyme complicatioed by multifacitaed appearance and non specific sx, prompting some med professionals to call it great imitator-looks like other diesease like lupus, fibromyalgia

several forms lab testing now avail

most used serological testing which measures specific levels of antibodies in blood, however, these tests often neg in early infec, and may not produce a sig quantity of antibodies til later stages, have high rates of false positives

PCR (polymerase chain reaction) also detects however not widely performed bc it often shows false negative results and CSF specimans, several labs perform PCR on ticks

avoid tick invested areas from may to aug

perform tick checks/proper removal w/in 24 hours

single antibiotic dose given w/in 72 hours after high risk exposure can prevent development of lyme

hx of previous lyme does not offer immunity

exposure can be reduced w/ simple landscaping like a gravel or wood buffer in between woods and recreation areas

community can dec lyme by dec hosts (rats)

antibiotics primary tx

since dx lyme, is based on clinc findings, it is often approp to tx px w/ early dx soley on basis od sx and a known exposure, newly dx cases are tx'd w/ antibiotics for 2-4 weeks and most px make an uneventful and complete recovery

early cases-prompt tx curative

some px w/ lume have fatigue, joint pain, and neuor sx exisiting for years despite tx

also called chronic lyme or post tx lyme dx ptld-depends on damage done initially

severity and tx may be complicated due to late dx, px w/ late stage lyme may have been shown to experience a level of physical disability equiv to that seen in CHF

in rare cases lyme is fatal

known as fok lun in samhita-1600's

very old

john snow-first instance of defining source of infection using epidemilogy

bacteria identified by robert koch in 1882

severe diarrehal sx

"rice water stool" (mucus)

5-20 L water loss/day

single flagellum

looks like a computer mouse

endemic in asia w/ 8 million cases annually 124,000 deaths (bangladesh, southern india, vietnam) etc

sever pandemics since 1817

entry into westerm hemishere

peru, alabame, chile 1991-1994

haiti-2010

gram neg, motile (flagella) bacillus

comma shaped bacterium

pilus (attachement) to epithelium

faculative anaerobe

free living and in gut

glucose and sucrose utilization (ferments)

oxidase-positive reaction in assay

capsule (polysaccharrides)-serotyping

gram neg-LPS antigenic variants used for serotyping

capsular polysaccharides used to serologically differntiate virbio cholerae strains, most prevalent strains O1 and O139

prior to 1993, O139

6th, 7th pandemics in haiti caused o1 serotype

more than 138 serotypes

pretty much only thing V cholerae will grow on

bile salts (no gram +)
ph 8.6 (high)

thiosulfate (sulfur)

citrate

sucrose

bromythmol blue

vibrio cholera-yellow (low pH) (sucrose fermentor)

20 species of vibrio have been identified

12 of these are responsible for human dx

v cholerae-potentially lethal intestinal infection

v vulnificus-fisherman; highly letahl systemic infection

cholera toxin-hypersecretion electrolytes and water

coregulated pilus(coregulated b/c only expressed when cholera is expressed)-adhearance to mucousal cells

accesorry colinzation-adhesion factor

hemagglutination protease (mucinase)-induces intestinal inflammation and degradation of tight junctions

siderophores-iron sequestration

neuramidase-inc toxin receptors

oral route

flagella; motility is required, swim through the mucus lining to the gut epithelial cells

toxin-corregulated pilus, attachment of bacterium to gut cells

HA protease ('detachase')-v cholerae is shed from the gut in diarrehal fluids-can cleave itself and flow out of guy

dispersal to other persons, contraminated food, water etc

-60% mortality rate

non invasive-attachement of v cholerae to gut epithelial requires interaction b/w bacterium's pilus and the microvilli ("brush border") on the gut cells surface

heat labile protein (enterotoxin) secreted by V cholerae into the lumen of the guy

binds to ganlisodie GM1 receptor located on surface of gut epithelial cells

5B monomores, and 2 alpha monomers, actual alpha unit causing interaction

elevates level of intracellular cAMP, stim release of electrolytes (K+,Na+) from the cell-pores of epithelium permanently open

cell water follows ion gradient

severe diarehal sx (rice water mucousy stool)

death by electrolytic shock

virbio like bacterium

promiscuous host range-major cause of diarrheal dx in animals, cattle, sheep, rodents, poultry, dogs, cats, birds

recently these bacteria have been implicated in human dx

gram neg encapsulated helical bacillis (curved or spiral rod)

motile (flagellated) (2!)

doesnt ferment sugar

microaerophillic (requires CO2 for growth)

too small to be easily observable by brightfield microscopy (reveleaved by scanning electron)

C. jenjuni-acute gastroenteritis

C. fetus systemic infection/bactermia, meningitis, and septic fetal abortions,

C. coli-procitis, gastroenteritis, septic fetal abortions

mucosal surface of intestine is ulcerated, edematous, bloody, inflammes (more acute than v cholerae)

monocytes are attracted to area

roles for cytopathic toxins, but enterotoxins and endotoxic activity have not been well defined

autoimmune dx thought to be elicited by antigentic cross reactivity b/w the capsule polysaccharides and sugar containing lipids on surface of neuronal cells

assoc w/ campylobacter

gastroenteridis

UTIs

neonatal meningitis

peritonitis

mastitis

septicemia

pneumonia

hemolytyic uremic syndrom

symbiotic relationship b/w ourselves and our gut flora

e coli is a normal consitiuent of our gut flora

less than 0.1% of culturable microflora in the gut is non patho eschericia coli

73 different locations were linked to food poisoning

hemolytic uremic syndrom (shiga toxin)

isolated to e coli

sickened over 700 people

171 hospitalizations, 4 deaths

gran neg bacillus

normal member of gut flora

faculative anaerobe

ferments sugars (glucose, lactose)

flagellated or non flagellated

often express pili and/or fimbriae

genetically diverse

-20% of genome common to all strains

LPS, flagellar, and capsular polysacchariddes (if cap polysachs produced) are used to serologically differentiate strains of E Coli

K antigens in capsule

O antigens in LPS

H antigens in flagellum

nicknamed swiss army knife of pathogens

EPEC
ETEC
EHEC
EIEC
EAEC
UPEC
NMEC

(enteropathogenic e coli)

site of action-SI

dx-infant diareha, watery diareha, vomiting, non bloody stools

pathogenesis-plasmid mediated histopathology, disruption of microvillus struc

enterotoxigenic e coli

site of action- small intestine

dx-travelers diareha, watery diareha, cramps, nausea, low grade fever

pathogenesis-plasmid mediated heat stable and/or heat labelle enterotoxins, hypersecretion of fluids and electrolytes

enterhemmorhagic e coli

site of action-large intestine

dx-inital watery diareha, followed by grossly bloody diareaha, cramps, little to no fever, may progress to hemolytic uremic syndrome (O157;H7)
pathogen-mediated by shiga toxins (stx 1, stx2) disrupts protein synth, A/E lesions

enteroinvasive e coli

site of action-large intestine

dx-fever, cramps, watery diareaha, may progress to dysentery w/ scant bloody stools

pathogen-plasmid mediated invasion and destruction of epithelial cells lining the guy

enteroaggregative e coli

site of action- small intestine

dx-travelers diareha, persistant watery diareha w/ vomiting, dehydration, and low grade fever

pathogen-plasmid mediated aggregative adhearance of rods (stacked bricks) shortened microvilli, mononuclear infiltration, hemorhage

extraintestinal e coli

site of action-uritogential tract

dx-inflammation of UT,

pathogen-produces specific adhesions P pIII, AAF/I, AAF/III, Dr

neonatal e coli

site of action-brain

dx-meningitic; majority of CNS infections in infants less than a month of age; often present in mothers and neonates GI tract

pathogen-most strains produce the K1 capsular antigen

effacement (destruction)of microvilli

type III secretion system; effector proteins alter cytoskelton

pedicle formation, stimulates apoptosis

Tir effect-receptor for bacterium

increases intraceullar cGMP (STa), cAMP (LT)

heat stable toxin (STa)

Heat labile enterotoxin (LT)

labile toxin (LT) similar to cholera toxin

opens ion channels in the intoxicated cell

loss of ions; intracellular water follows osmotic gradient-diareha

shiga toxins: disrupt synthesis of proteins in infected cell; inactivates ribosomes

60MDa virulence plasmid

**Death w/in 3-5% px with hemolytic uremic syndrom

30% of HUS px can have lifelong CNS and renal impairment

similar to shigella

invades into cytoplasm of cell

"rocket" motility, polymerization of action

likely sim phenotypes b/c it invades wall

Inv plasmid: encodes for invasion functions similar to the Inv plasmids of Shigella spp

invades much like shigella

whole groups of pilli can bind to each other

plasmid-mediated adhearance

stacked brick colonization-binds to itself

bundle forming pilli

shortened microvilli evident

intestinal hemorrhage-ulcerations and breaks in guy lining

dont really care for guy

most strains of e coli can produce UTIs

Type I fimbriae-adheres to bacteria to UT epithelium