Exam 2 Flashcards
Listeria monocytogenes Characteristics
G+B Non-branching Short chains, pairs CAT+ CAMP+ Weak beta hemolysis Facultative, high NaCl Tumbling motility Wide temp and pH range
Listeria spp.
G+B
Aerobes
Non spore-forming
Listeria monocytogenes pathogenesis
Contact via contaminated food/water
Intercellular pathogen - avoid clearance by humoral immunity - T cell defect patients highly susceptible
Bacterial endotoxin: listeriolysin O (activated by phagolysosome acidity)
Moves cell to cell via filipod
Listeria monocytogenes clinical disease
Neonate: early onset - in utero - abortion, stillbirth, premie
Late onset - 2-3 weeks - meningitis or meningoencephalitis with septicemia
Adult: asymptomatic, flu-like, meningitis, bacteremia
Erysipelothrix rhusiopathiae characteristics
G+B Non-spore forming Microaerophilic or high CO2 CAT- Non-motile H2S+
Erysipelothrix rhusiopathiae pathogenesis
Neuramidase: attachment and penetration into epithelial cells
Capsule
Found on swine and turkeys, zoonotic infection - occupational risk: meat processors, pig farmers, poultry workers, fish handlers and vets
Erysipelothrix rhusiopathiae clinical disease
Erysipeloid - localized skin infection, violet, pruritic (itchy) rash on fingers and hands
Corynebacterium spp characteristics
G+B Aerobic "Coryneform" club shaped bacilli CAT+ Non-motile Fermenters Metachromatic granules with special stains
Corynebacterium spp. Pathogenesis
Found in plants, animals, and colonize human skin, upper respiratory tract, GI and urogenital tract
Opportunistic pathogens
Corynebacterium diphtheriae characteristics
Pleomorphic G+B with metachromatic granules
4 biotypes: belfanti, gravis, intermedius, mitis
Corynebacterium diphtheriae pathogenesis
Diphtheria toxin - major virulence factor, exotoxin produced at site of infection and spreads thru blood to produce systemic symptoms
Coded for by tox gene which enters organism via lysogenic phage
Classic A-B toxin
Corynebacterium diphtheriae clinical disease
Diphtheria: clinical presentation is determined by site of infection, immune status of patient, virulence of organism
Respiratory: malaise, sore throat, fever, exudative pharyngitis that develops into thick pseudomembrane (adheres to underlying tissue), systemic illness in severe cases: myocarditis, congestive heart failure, cardiac arrhythmias
Cutaneous: acquired through skin contact, papule develops turning into chronic non-healing ulcer
Corynebacterium jeikeium characteristics
Opportunistic pathogen in immuno-compromised pt. and hospitalized pts.
Corynebacterium urealyticum
Urinary tract pathogen, immunosuppressed, genitourinary disorders, previous urological procedures, or antibiotic therapy.
Produces urease which makes urine alkaline –> renal stones
Corynebacterium pseudotuberculosis and ulcerans
Both closely related to diphtheriae
Can carry diphtheria gene
Pseudotuberculosis infections are rare
Ulcerans causes same disease as diphtheria
Mycobacterium spp. characteristics
Acid fast bacilli, cell walls rich in lipids - mycolic acids - cells won’t decolorize
Provides resistance to many antibiotics, antigenicity, and clumping
Non-motile
Aerobic
Non-spore forming
Slow growth
Runyon Classification
For non-tuberculosis mycobacteria
Slow-growing photochromogens (pigment in exposure to light)
Slow-growing scotochromogens (pigment in absence of light)
Slow-growing non-pigmented
Rapidly growing
M. Tuberculosis complex - slow-growing non-pigmented or light tan color
Slow-growing photochromogens mycobacteria
M. kansasii
M. marinum
Slow-growing scotochromogens mycobacteria
Mycobacterium gordonae
Slow-growing non-pigmented mycobacteria
M. avium
M. intracellulare
Rapidly-growing mycobacteria
M. fortuitum
M. chelonae
M. abscessus
Mycobacterium tuberculosis
Intercellular pathogen taken into resp. tract
Phagocytize do by macrophages where it grows. Macrophages secrete TNF and IL-12 which bring on intercellular killing
Granulomas (necrotic mass trapping bacteria) are formed. A small one is killed. A large one be coated with fibrin which protect the bacteria from macrophage killing
Humans only known reservoir
Spread thru inhalation of infectious aerosols
M. tb clinical disease
Most infections in middle to lower lungs, can be anywhere
Diagnosis with x-ray and positive PPD skin test
Neisseria spp. Characteristics
G-DC (kidney beans) Aerobic OXI+ CAT+ Oxidize carbs Non-fermenters Non-motile Non-spore forming
Neisseria gonorrhoae characteristics
G-DC Oxidize glucose (g) Fastidious - require cystine CO2 MTM media
Neisseria meningitidis characteristics
G-DC
Oxidize glucose and maltose (g,m)
Neisseria structure
G- cell wall
N. meningitidis - polysaccharide capsule - allows for antigenic aero typing (A, B, C, Y,
N. gonorrhoae lacks a capsule
Pili - attachment and conjugation (pathogenicity and virulence)
Por A and B integral proteins - virulence factor that interferes with phagolysosome fusion
(gonorrhoae only has Por B)
OPA proteins - membrane proteins that mediate binding to epithelial and phagocytic cells; cell-cell signaling - clinical disease and virulence
Mycobacterium leprae characteristics and clinical presentation
slow replication, long incubation period
symptoms can develop 20 yrs. after infection
2 kinds: tuberculoid leprosy - strong cellular response, lymphs and granulomas, few bacteria, cytokines induced, macrophages, phagocytosis, bacillary elimination
lepromatous leprosy - strong Ab response, no cellular, many bacteria in dermal macrophages and peripheral nerve Schwann cells * most infectious form
person-person spread
lepromin skin test - injection of inactivated leprosy bacillus under skin to detect infection
Mycobacterium leprae clinical disease
leprosy - chronic infection affecting skin and peripheral nerves, disease is host response
tuberculoid - milder, hypo pigmented skin macules, less organisms
lepromatous - disfiguring skin lesions, nodules, plaques, thickened dermis, involvement of nasal mucosa, more bacteria
Mycobacterium avium/MAC
MAC - Mycobacterium avium complex
disease in immunocompromised
pulmonary disease seen in immune-competent pts.
tons of bacteria
ingestion of bacteria, not person-person, contaminated aerosols
replication in localized lymph nodes, then systemic spread
Enterobacteriaceae characteristics
G-B FA CAT+ OXI- ferment glucose reduce nitrate no spores soil, water, vegetation, normal flora peritrichous pili if motile fimbriae - adherence conjugative pili
3 kinds of Enterobacteriaceae pathogens
- strict pathogens
Salmonella Typhi, Shigella, Y. pestis - Opportunistic pathogens
K. pneumoniae, P. mirabilis - Acquired virulence pathogens
E. coli gastroenteritis (E. coli 0157)
Enterobacteriaceae structure
LPS - major cell wall Ag, heat stable
Made up of outermost O polysaccharide, core polysaccharide, Lipid A
3 antigen groups used for serological classification of Enterobacteriaceae
- Somatic O polysaccharides
- Capsular K antigens (block O polysaccharide, heat-labile)
- Flagellar H proteins (present in motile pathogens, heat-labile)
3 virulence factors of Enterobacteriaceae
- Capsule - avoid phagoctosis
- Endotoxin - Lipid A, activate complement, cytokine release, leukocytosis, thrombocytopenia, DIC, shock and death
- Type III secretion system - allow bacteria to secrete proteins into phagocyte –> destroys proteins needed for phagocytosis; suppresses cytosine production –> lowers inflammatory response and prevents complement binding
ETEC
Enterotoxigenic E. coli
young children, travelers (water/food, high innoculum)
enterotoxin - Lipid A
genes on plasmid
need to colonize AND produce toxins to cause disease
EPEC
Enteropathogenic E. coli
infants (daycare –> diapers)
person-person spread (lower innoculum)
pathogenicity island - regulates attachment and destruction
destruction of microvilli
EAEC
Enteroaggregative E. coli
infants, travelers
auto-agglutinate - protection from Abs and phagocytosis
chronic, watery diarrhea
EHEC
Enterohemorrhagic E. coli
most common strain
young children (can develop HUS - kidney failure)
from unpasteurized dairy, contaminated veggies, undercooked meat, chopped meat, apple juice
E. coli 0157 - acquire Shigella toxins via lysogenic bacteriophage
EIEC
Enteroinvasive E. coli
invade and destroy colonic epithelium
very closely related to Shigella
Rare in the US
Extraintestinal E. coli infections
UTI - adhesions prevent elimination via voided urine
Neonatal meningitis - infants <1 month, K1 capsular Ag, common in GI tracts of pregnant women and newborns
Septicemia 0 originates from GI or UT
Salmonella Clinical Disease
Gastroenteritis - most common form of Salmonellosis, consumption of contaminated food
nausea, vomiting, cramps, diarrhea (no blood)
Septicemia
Typhoid fever - caused by S. typhi and a mild form by S. paratyphoid
macrophages transport bacteria to the liver, spleen,a dn bone marrow
fever, headache, myalgias, malaise, anorexia
chronic colonization
humans only
Shigella
4 spp.
bacillary dysentery
invasive - colon lining, adherence, invasion, replication (genes and plasmid)
dysenteric strains - enterotoxic Shigella toxin - causes diarrhea (A-B)
Renal failure
only humans, mostly children
person-person spread
abdominal cramps, fever, watery diarrhea, increased WBC count, blood and pus in stool
Yersinia pestis
Plague: urban plague - rats from fleas
sylvatic plague - squirrles, rabbits, field rats, domestic cats
2 plasmids coding for virulence genes:
F1 - antiphagocytic protein
Plasminogen activator protease gene - degrades complement, preventing opsonization and phagocytosis; degrades fibrin clots –> spread
Clinical disease:
bubonic plague - bitten by infected flea, fever and painful bubos, bacteremia
Pneumonic plague - fever, malaise, pulmonary signs, highly infectious aerosol
Yersinia enterocolitica
Enteric pathogen
enterocolitis - diarrhea, fever, abdominal pain, can mimic appendicitis
blood transfusion-related bacteremia and endotoxic shock
Yersinia spp.
Y. pestis
Y. enterocolitica
Type III secretion system
ALL infections are zoonotic
Klebsiella
prominent capsule - mucoid colonies
K. pneumoniae and K. oxytoca - community and nosocomial lobar pneumonia; also wound, soft tissue, UTI
K. granulomatis - granuloma inguinale –> called donovanosis
subcutaneous nodules develop into painless granulomatous lesions that can extend out and coalesce. STI or via genital trauma
Proteus
P. mirabilis - most common
UTI, produces urease which makes urine alkaline –> renal stones
produce fimbria for adherence
Campylobacter Characteristics
G-B spiral-shaped (not spirilium!) Microaerophilic (CO2) No fermentation or oxidation of carbs Polar flagella 25 spp.
G- cell wall, LPS major cell wall Ag
Somatic O polysaccharide, heat-labile capsular and flagellar Ags.
Helicobacter Characteristics
G-B spiral-shaped (not spirilium!) Microaerophilic (CO2) No fermentation or oxidation of carbs Most OXI+ Most CAT+ Ferment amino acids
Campylobacter Diseases
Gastroenteritis - C. jejuni or C. coli
an acute enteritis with diarrhea, fever, abdominal pain, bloody stool, chronic in immunocompromised
Septicemia/systemic infections (arthritis, septic abortion) - C. fetus
Campylobacter jejuni
Adhesins, cytotoxic enzymes, enterotoxins 0 not only cause of virulence (strains lacking these are still virulent)
Seen in pts. undergoing treatment for gastric acids
GI disease - ulcerated, edematous, bloody crypt abcesses
Campylobacter fetus
heat-stable capsule-like protein (S protein) - prevents complement binding –> only virulence factor
Helicobacer pylori
G-B spiral (not spirilium!) polar flagella - highly motile urease OXI+ CAT+ ferment amino acids LPS - lipid A low endotoxin activity CAUSE ULCERS
