Gram Positive Cocci
Treatment / Characteristics / Associated Disease(s) / Pathogenesis / TreatmentStaphylococcus aureus / Gram + cocci in clusters,immotile human skin and nares,body walls off infection w/a fibrinous barrier; S. aureus causes pus formation. / Invasive: suppurative skin infections: minor trauma pimples ,carbuncles, impetigo; major osteomyelitis, fasciitis, cellulitis.
hematogenous inf., nosocomial infection.
Toxinoses: Food Poisoning (enterotoxin), exfoliative skin disease (Ritter’s disease of newborns), TSS / Multifactorial; secrete 4 hemolysins that lyse cells; -hemolysin lyses cell similar to pore form. by complement, also:coagulase +, exfoliatin. Protein A is a surface molecule that binds IgG to camouflage the bacterium. Also able to respond to env. w/signal molecule. / penicillin
vancomycin
[erythromycin]
(Many strains are multi-abx resistant.
and make -lactamase)
Staphylococcus epidermidis / Gram + cocci in clusters, human skin (always), / Opportunistic infections, large number of nosocomial infections: bacteremia, endocarditis, endophthalmitis, osteomyelitis (following surgery), infections of indwelling foreign devices, neonatal necrotizing enterocoloitis. / Coagulase negative
Staphylococcus saprophyticus / Gram + cocci in clusters, skin/genitourinary tract / Infections outside of hospital, causes 20% of all urinary tract infections in young women. / Coagulase negative
Streptococcus pyogenes
(Group A, -hemolytic) / Gram + cocci in chains, catalase neg., Group A causes most strep disease, asymptomatic carriers, causes suppurative infections. / Suppurative: Pharyngitis, Scarlet Fever, erysipelas, streptococcal pyoderma (impetigo).
Non-suppurative: Acute Rheumatic Fever, Acute Glomerulonephritis. / Surface molecules confer adherence to tissues and resistance to phagocytosis.
M-protein(prevents phag.), Protein F (adherence-fibronectin), Fc receptor (like Prt.A), C5a peptidase, etc. Secreted exotoxins: erythrogenic toxin, Streptolysin S, Streptolysin O, Streptokinase, DNAse. / Very sensitive to penicillin.
If patient is allergic, give erythromycin.
Streptococcus agalactiae
(Group B, -hemolytic) / Gram + cocci in chains, catalase neg., lower GI tract & female genital tract. / Puerperal sepsis (after childbirth) , neonatal meningitis (early onset w/50% mortality or late onset w/20% fatality) / Capsular polysaccharide (prevent phag.), Hemolysin (like streptolysin S), IgA receptor (camouflage), Fibronectin binding protein (adherence). / penicillin
vancomycin
chloramphenicol
Viridans Streptococci
(-hemolytic) / Gram + cocci in chains, catalase neg., oral cavity (up to 60% of normal oral flora) / dental caries, subacute bacterial endocarditis (on pre-existing heart valve lesions),enter bloodstream via decayed teeth or following oral surgery. / penicillin
Enterococcus faecalis
(-hemolytic, non-hemolytic) / Gram + cocci, low pathogenicity, normal flora of human gut, very hardy. / subacute bacterial endocarditis, female urinary tract infections, peritoneal abscess, bacteremia (from above foci). / Antibiotic resistance to every known antibiotic due to conjugal transfer of antibiotic resistance genes within and across species / ???
Streptococcus pneumoniae
(“the pneumococcus”) / Gram +, encapsulated, lancet shaped cocci in pairs, usually community acquired, sporadic.
Transmitted by droplet nuclei or aspiration by carrier. Facultative anaerobes, -hemolytic. / Pneumonia (Lobar and Bronchopneumonia,most common cause of meningitis in adults, most common cause of otitis media and sinusitis in children, can cause septicemia, esp. in the very old or very young. (Immunity to reinfection is type-specific against capsule.) / Capsule confers path: inhibits phagocytosis by inhibiting alt.pathway, must be present for virulence. Capsule also stimulates production of type-specific opsonic Ab that results in killing by PMNs. No toxins involved in path. 85 different serotypes. / penicillin
amoxicillin
cephalosporins
vancomycin
Vaccine for people at risk available.
Gram Positive Rods
Organism / Characteristics / Disease(s) / Pathogenesis / TreatmentListeria monocytogenes
(see HO, lots of details for this one) / Gram+, non-encapsulatedrod w/a characteristic “tumbling” motility, facultative intracellular parasite, grows under many conditions, found nearly everywhere, transmitted through improperly pasteurized milk/products, oral-fecal contamination of any source (ie- H20 contamination, vegetable fertilized w/manure, meat, etc). / Listeriosis is disease. Rarely causes disease but when it does is severe esp to fetus, newborn, pregnant women and the immuno- compromised. 70-90% fatality if untreated, 30-50% fatality w/treatment depending on status of host and clinical signs. Can be carried in GI tract or female genital to lead to disease. Is able to enter a wide variety of cells where it can survive and multiply. Immunity to re-inf w/ survivors. Septicemia, meningitis, abscesses, granulomas, lymphadenitis. Lead cause of meningitis in CA/renal tp patients / Extracellular product listeriolysin O is responsible for pathogenicity- a cytolysin that specifically dissolves the endosomal membrane so that it evades the major anti- bacterial activity of the cell, this way the org. can also get into cytoplasm. Cell surface virulence includes Internalin for attachment and invasion and Act A for directional actin polym. of host cell’s actin. Actin polym. allows bacteria to move in cytoplasm and is required for cell-cell spread, also makes it resistant to humoral immunity. / Ampicillin,
penicillin with an aminoglycoside,
erythromycin.
Use only pasteurized milk products b/c of this bacterium!!!
Bacillus anthracis / Gram +, sporeforming, non motile rod with characteristic square cut ends (boxcar), encapsulated, spores can live in the soil for 30 years, found carried in GI tract of animals, transmitted by spores or respiratory droplets. / Anthrax (cutaneous or inhalational).Mostly a disease of animals or people who work with animals.Cutaneous enters thru cut on skin, causes a malignant pustule that is a necrotic black lesion then rapidly disseminates and causes death very quickly. Inhalational is from organisms directly to lung that release exo-toxin and cause pulmonary necrosis, septicemia, meningitis and death w/in 24h. / Exotoxin produces pathogenesis. Toxin is a heat labile protein composed of 3 components: protective antigen, lethal or toxic factor and edema factor. Polypeptide capsule made exclusively of D-glutamic acid gives anti-phagocytic activity but does not stimulate protective antibody / Vaccine (but is only 50% eff)
Penicillin and tetracycline are effective only when given early
Bacillus cereus / Gram+, motile, non encapsulated, beta hemolytic, exists as a saprophyte in water and soil, trans. in contaminated rice or meat dishes / Self limiting type of food poisoning. Incubation period and clinical sx. resemble staph. food poisoning. Can also cause disseminated, usually fatal, disease in immuno compromised pts.(usually post-operatively). / Secretes enterotoxins
Corynebacterium diphtheriae / Gram +, non sporeforming, non motile, vy. distinct (beaded, barred or clubbed), facultative anaerobes, obligate parasite of humans, carried in URT, transmitted by droplet nuclei or contaminated milk, people can be carriers. / Diphtheria. Fever, chills, pharyngitis, cervical lymphadenitis, massive neck edema (severe cases) and a thick, closely adherent dirty gray pharyng., tonsillar or laryng. pseudomembrane
Death due to resp. paralysis or myocarditis. Cutaneous diphtheria results in an ulcerative lesion w/a dirty gray pseudomembrane. W/both there can be toxemic degeneration and death. / K antigen on surface is anti-phagocytic. Exotoxin is of 2 polypeptide fragments: B fragment is for transport into cell and A frag ment is toxin for ADP-ribosylation and inactivation of elongation factor EF-2 which inhibits protein synthesis. Lysogeny w/ a beta prophage carrying the tox gene is essential for toxigenicity. / Vaccination prevents disease
Active disease: give anti-toxin immediately, penicillin or eryth
romycin for killing bacteria.
“Diphtheroids” / Same habitat, may have same morphological and biochemical properties as C.diphtheriae but they do not produce exotoxin / Can cause septicemia in rare instances in immunosuppressed individuals with a high fatality rate. / Often have multiple antibiotic resistance, but do not produce exotoxin
Gram Positive, Anaerobic, Sporeforming Rods
Organism / Characteristics / Disease(s) / PathogenesisClostridium botulinum / Gram+, anaerobic, spore form- ing, multiplies in uncooked meat, sausage, fish and badly canned items, dx. by animal injection, cultures show characteristic “light bulb” appearance. Spores do not produce toxin, only vegetative form does. / Botulism. Caused by intoxication w/bacteria. Clinical sx. 18-36h after ingestion, ptosis, mydriasis, blurred vision, dysphagia, dysphonia, urinary retention, muscle weakness (descending), respiratory paralysis. Death can occur w/in 18h. This results from Ach presynaptic blockade. Infant Botulism results in floppy infant, may be cause of SIDS in some cases. / Botulinus toxin causes path. Released by lysis of bacterial cells in medium. Toxin has two subunits:H-chain causes receptor mediated endocytosis by host cell, once in cell the H and L-chain are separated and the L-chain moves by retrograde transport to the presynaptic terminal where it prevents fusion of the synaptic vesicles w/the presynaptic membrane. All toxins are destroyed by boiling at 100C for 10 minutes. / Free toxin can be inactivated with a specific antiserum. Give a polyvalent antitoxin. Do not give penicillin b/c it causes cell lysis and more toxin.
Clostridium tetani / Gram+, anaerobic, spore formi-ing, found all over the place, typical entry through wounds (puncture wound or laceration, but also burns, ulcers, cpd fx, operative wounds, injection sites of IVDAs, Dx. is clinical, appear on culture as gram+ rods w/spore formation at tip forming a “drumstick” / Tetanus. Caused by intoxication, may take several days to weeks for symptoms to occur. Onset of sx. may be muscular contractions in the vicinity of the wound followed by spastic contraction of the masseter muscle (trismus) resulting in “locked jaw”, generalized rigidity and severe spasms of the limbs and trunk. Later signs: risus sardonicus, spasmic contractions of back(opisthotonus) and of the resp.muscles which may lead to death. / Secretes tetanus toxin which is a dimer similar to botulinus toxin (H and L chain) L chain functions as a synaptobrevin on the surface of synaptic vesicles that inhibits their fusion with the presynaptic membrane. Tetanus toxin specifically blocks the inhibitory neurons of spinal motor neurons preventing release of GABA and glycine which results in uninhibited transmission of excitatory impulses and muscular spasms. / Immunization @ 2,4,6 mos. and boosters every 5-10 y.
Antitoxin + immune globu-lin given to wounded people w/o immun. immediately!
Clostridium perfringens / Gram+, anaerobic, spore forming, occur normally in soil and sewage, normal in human GI, box shaped organisms with gram stain, positive blood cultures(for gas gangrene), found also in feces for other infections / Gas gangrene. Destroys tissues esp. muscle,Infects poorly perfused, injured tissues, incubation 6-72h, severe edema, bronze discoloration, bullous lesions w/dark thin fluid, then H2 gas production leading to crepitations, ischemia, shock and death. Most common organism to cause gas gangrene.
Also: Anaerobic cellulitis, uterine infection, necrotizing enteritis, food poisoning (self limiting diarrhea). / Produces extotoxins. Most important toxin is -toxin which cleaves lecithin in host cell membranes and is lethal and necrotizing on injection. Perfringolysin O (similar to strep-tolysin O, pore complexes). The combined action of -toxin and streptolysin O may be the cause for the intravascular hemolysis associated w/ infections. b-toxin important in necrosis of necrotizing enteritis. Spores in food germinate & release toxin in food pois. / surgical excision of inf. skin and muscle, limb amp utation, hyper-baric O2. Abx to well perfused tissues, no time to wait for cultures! Surg.for bowel in enteritis.
Clostridium dificile / Gram+, anaerobic, spore forming, normal commensal of human gut, results from superinfection following antibiotic treatment / Pseudomembranous colitis. Diarrhea and toxic megacolon. Endoscopy shows multiple small pseudomembranous colon plaques. Milder form is antibiotic associated diarrhea w/ same clinical findings but less severe / Produces two heat labile toxins: A and B. The toxins are released by vegetative cells and together cause fluid loss, mucosal damage and necrosis of intestinal mucosa. Toxin can be id by ELISA. / Stop previous abx tx. Vancomycin or metronidazol to stop inf. Surg-ery for megacolon
Gram Negative Coccobacilli
Organism / Characteristics / Disease(s) / Pathogenesis / TreatmentBordetella pertussis / Gram neg, coccobacillus, non motile, non sporeforming, piliated, LPS, obligate aerobe, slow growing, hard to grow, human respiratory tract, no known animal or environment-al reservoir, transmitted by respiratory droplets, highly communicable, mostly children / Pertussis (whooping cough). 4 phases: 1. incubation; 2. catarrhal (mild cold-like sx. , mild cough of severity,most infectious phase)
3. paroxysmal (severe, forceful, spasmodic coughing w/ “whoop” following and then vom-iting, complicated by otitis media, seizures, apnea, pneumonia); 4. convalescent (less fr. paroxysms, recovery). 1% death rate, mental retardation and paralysis can occur. / Attaches (firmly) to ciliated resp.epithelial cells(using FHA,pili and peritactin), secretes toxins to inhibit phago.cells (adenylate cyclase toxin, pertussis toxin )& inhibit muco-ciliary defense(tracheal toxin), multiplies and causes local damage, systemic disease results (lymphocytosis, insulin, glycemia) See HO for details of toxins. / Erythromycin for active disease.
Vaccination to prevent disease. Vaccine can cause some se’s but is safe and prevents epidemics.
Haemophilus influenzae / Gram neg, coccobacillus, non spore, non motile, encapsulated and nonencapsulated strains, fastidious, facultative anaerobe, requires hemin and NAD, found in human respiratory tract, transmitted by respiratory droplets. / Meningitis, epiglottitis (in kids), not seen often any more b/c of vaccine, 75% unencapsulated causes otitis media, sinusitis, bronchopneumonia, 5% encapsulated causes pneumonia, epiglottitis, bacteremia, meningitis
Most common from 3mos to 4 yr after maternal ab’s have worn off and T cell response not active. Complications are severe. / Capsule is antiphagocytic major virulence factor (PRP polymer, most adults have anti- PRP Ab), pili may have a role in attachment, LPS, outer membrane proteins, IgA protease (specific role not yet established) / Vaccination
For active disease give cephalospor-ins, ampicillin + chloramphenicol.
Gram Negative Cocci
Name / Characteristics / Disease(s) / Pathogenesis / TreatmentNeisseria meningitidis / gram-, diplococci, fastidious, habitat is human mucosal surfaces, poor environmental survival, symptomatic & asymp inf. Spread by respiratory droplets. Detect by gram st, serum Ag, culture, clinical dx. / Meningococcal disease: meningitis and/or septicemia(fever,ha,chills, malaise, wkness, hemorrhagic skin lesions/petechiae/purpura, DIC, Thrombocytopenia, leukocytosis, hypotension, septic shock (LPS-A). Can be epidemic, bacteremia in susceptible people (asplenic pts, children), carrier state in others / Attaches to non-ciliated cells of the nasopharyngeal mucosa and undergo TRANSCYTOSIS to cross the basement membrane. Features: Pilus(attachment), IgA1 protease(cleaves IgA), antiphagocytic capsule, LipidA(septic shock). / IV antibiotics, manage complications, prophylaxis during epidemics
Neisseria gonorrheae / gram- diplococci, fastidious, human mucosa/poor environ. survival, sympt/asympt inf.
Spread by sexual contact or perinatal inf. Gram st of exudate in males can dx. but for sure culture to confirm from any source. / Gonorrhea: Urethritis (males), cervicitis (females), rectal inf, pharyngeal inf, ophthalmia neonatorum (mother to infant gonococcal conjunctivitis).
Complications: PID, Disseminated gonococcal infection (DGI, only 0.5-3% of inf) leading to arthritis, dermatitis, tenosynovitis(Lover’s heels), fever, often mild systemic toxicity. / Attachment: by a pilus that shows Ag variation to effectively evade the immune system and by an opacity protein that also has Ag variation, Lipooligosaccharide(LOS) toxic also shows Ag variation, IgA1 protease to evade IgA on mucosal surfaces, P1 porin shows resistance. Inflammation is intense, dissemination can occur but not as prone as in N.meningitidis / Uncomplicated ceftriaxone + doxycycline.
Many pcnase producing strains, tx for chlamydia too, tx for sexual partner, no vax, use a condom
Gram Negative Rods (Enteric)
Organism / Characteristics / Associated Disease(s) / Pathogenesis / TreatmentVibrio cholerae / gram-,curved rod, single polar flagellum(motile), endemic, epidemic, pandemic, trans in contaminated food/H20 (fecal-oral trans),lives in brackish water/shellfish, human is transitory habitat. / Cholera: Inf. is asymptomatic to acute in nature, can be spread by asymp people, early signs: vomiting, cramps, then PROFUSE secretory diarrhea (rice water stools), massive fluid loss of 10L/day leads to dehydration, electrolyte deficiency and hypovolemic shock. W/o tx. 60% fat., w/tx. only 1% fat. / Raising pH of stomach encourages infection.
1)colonization: ingestion, gastric acid barrier, attachment to sm.bowel (microvilli)
2) cholera toxin: ADP ribosylates G prt. to “turn on” adenylate cyclase, loss of salt and H20 by diffusion into lumen, loss of bicarb can lead to acidosis. / Replace fluids & electrolytes po or iv, tetracycline duration, vaccine under dev. Tx. is very effective & easy to give.
Vibrio parahaemolyticus / Halophilic (salt loving), marine habitat (coastal waters) / Food poisoning: undercooked seafood, causes secretory diarrhea
Vibrio vulnificus / Seawater / Septicemia in compromised host, cellulitis in healthy host
Campylobacter jejuni / gram-,curved,spiral or comma shaped rods, motile, micro-aerophilic, worldwide zoonosis in GI tract of dom. animals, trans by cont food/water, common, est 2Mcases/yr in US / Common cause of diarrhea.
Acute enteritis: diarrhea, malaise, fever, abd. pain. Range of diarrhea from loose to watery to bloody. Ususally self limiting, bacteremia rare, dx. by stool culture. / Pathogenic mechanisms uncertain / Fluid and electro-lyte replacement, antibiotics may be indicated(bloody stool), usually no tx is necessary.
Campylobacter fetus / fairly rare / Systemic disease in immunocompromised host
Helicobacter pylori / gram-,spiral rods, motile, produce urease, habitate the gastric epithelium / Gastritis/ulcers: thought to be cause of much gastritis and predisp to stomach CA, abx. tx. against clears up ulcers and gastritis. / Virulence: motility, urease, cytotoxin, exact cause of inflammation is unknown, infection remains for life if not treated. / triple tx: pepto, metronidazole, amoxicillin.
Salmonella enterica
(serotypes referred to as if they are species) / Gram- rods, motile, facultative intracellular, usually aquired by contaminated food or animals esp. poultry meat or eggs, infections are typically animal associated, fecal oral transmission as well. / Acute enterocolitis: Most common disease syndrome of salmonella, follows 6-8 hr incub-ation, most pts. have nausea, vomiting, diarrhea. Fever and abd cramping also common, inf involves small bowel and colon (different site from shigella), Fecal PMN’s are present, dx. by stool culture for enteric pathogens, death is rare. Infections can spread beyond intestinal mucosa to produce bacter-emia and seed distant tissues that can result in later focal infections (osteomyelitis in sickle cell pts. occurs w/ increased frequency) / Invades epithelial cells by contact w/ micro-villi of host, then bact cell assembles invasomes (invasion organelles) which triggers host cell memb. ruffling, the bact then shed their invasomes followed by host cell uptake. Salmonella can turn on and off genes according to if they are in a host cell or not, PhoQ is a sensor molecule (ex: low pH inside a phagolysosome) that regulates genes for transcriptional regulation and turns off other genes. Pag C is essential for resistance to killing by macrophages. / Antibiotics not recommended for uncomplicated enterocolitis, ceftriaxone for sepsis. Prevent w/ public health measures (ie restaurant safety) no vaccine available
Salmonella typhi / Gram - rods, motile, facultative intracellular, infects only man, get from people who are chronic carriers and excreters (Typhoid Mary) a condition that occurs in 1-3% of untreated cases. Fecal oral transmission / Typhoid fever (enteric fever): Incubation 1-3 weeks, gradual onset of fever, abd pain and hepatosplenomegaly, duration usually 4 weeks w/o tx. Dx. by culture of blood, bone marrow and stool. bone marrow gives the highest yield of organisms b/c it is a systemic infection of mononuclear phagocytes. Death may occur despite use of antibiotics b/c of the fatal comp-lication of intestinal perforation and peritonitis / S. typhi first invades small bowel epithelial cells or M cells in Peyer’s patches trans-cytosis across epithelial cellsendocytosis by lamina propria M. Bact survive in “spacious phagosomes” and reach systemic circulation via thoracic duct reticuloendo-thelial system (phagocytes in liver, spleen and bone marrow). Gall bladder inf leads to the chronic carrier state. Inf dose is large. / Ceftriaxone (1st ), ampicillin or co-trimoxazole if not severe. Prevent by public health measures. Killed and live -attenuated vaccine available.
Shigella
(dysenteriae, flexneri, boydii or sonnei) / Gram- rods, not normal flora, facultative intracellular,motile exclusive to primates, vy few needed to infect, evade host def like gastric acid, fecal-oral transmission: The Four F’s:
food, fingers, feces, flies. Only person to person. / Shigellosis: suspect in any diarrhea lasting > 48 hours. Abd cramps, may have fever. Stools have PMN’s, blood, mucous. 1wk is avg. time. Dx. by stool culture, produce disease at very low inoculation. / Intracellular, 1st invades M cells of gut lymphoid follicles, kill resident macrophages invade intestinal epith cells on basolateral surface, then spread cell-cell. Use host cell’s actin to rocket from cell-cell (like Listeria), express IcsA protein. Invasion plasmid is essential for pathogenicity. Secrete shiga toxin, causes endothelial damage. Expression of proteins is temp. controlled.
Gram Negative Rods (Nosocomial)