Gram-Positive Bacteria Flashcards
is Gram-positive Cocci
- Staphylococci*
- Streptococci*
- Enterococci*
staphylococci
gram-positive cocci that gorw in grape-like clusters
- Staphylococcus aureus* - one of the most important human pathogens
- Staphylococcus epidermidis* - normal inhabitant of skin, nose, and mouth of humans, adept at attaching and growing on prospthetic divices such as intravenous catheters and prosthetic joings, coagulase-negative
- Staphylococcus saprophyticus* - urinary tract infections in young women
Staphylococcus aureus
facultative anaerobe
most virulent of the staphylococci
Toxic shock syndrone toxin 1 (TSST-1)
causes staphylococcal toxic shock syndrome
grow at isolated site - eg vagina of a menstruating woman
toxin produced and enters bloodstream
causes systemic effects in the absence of bateremia
exotoxin instead of endotoxin
superantigen
causes proliferation of entire subsets of T cells (those with T cell receptors with specific Vbeta domains)
results in the release of large amounts of cytokines such as interleukin-1beta and tumor necrosis factor - alpha
cytokines cause fever, shock, and organ failure
Staphylococcal enterotoxins A-E and G-I
cause staphylococcal food poisoning
act directly on neural receptors in the upper gastrointestinal tract -> stimulate vomiting center in the brain -> cuase vomiting 2-5 hours after ingestion
toxins are resistant to boiling for 30 minutes as well as digestive enzymes
superantigens
exfoliatin
causes scalded skin syndrome
distrupts intercellular junctions in the skin -> splitting of the epidermis between the stratum spinosum and stratum granulosum
Staphylococcus aureus
alpha-toxin (alpha-hemolysin)
a factor that causes the lysis of red blood cells when bacteria are grown on blood agar plates
a lipid-binding toxin that inserts into lipid bilayers of mammalian cells and forms pores -> cell death and tissue destrcution
thought to lyse other types of host cells or act as transporters during infections
Staphylococcus aureus
Panton-Valentine leukocidin (PVL)
pore-forming toxin associated with many community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) strains
throught to contribute to cell lysis, resulting in severe, necrotic infections caused by mant CA-MRSA strains
PVL gene is carried by a phage
Staphylococcus aureus
coagulase
binds to prothrombin to fomr a complex that initiates the polymerization of fibrin to form a clot
contributes to the fibrin capsule surrounding many abscesses
prevents neutrophils from accessing bacteria
Staphylococcus aureus
Protein A
binds to Fc portion of IgG molecules
prevents antibody-mediated clearance
Staphylococcus aureus
furuncle and carbuncle
furuncle - a boil caused by the blockage of a hair follicle or sweat gland, subsequently becomes infected
carbuncle - when infection spreads from a furuncle and causes the formation of multiple abscesses in adjacent tissue
Staphylococcus aureus
joint and bone infections
if bacteria gains access to the bloodstream, it can cuase infections at distant sites such as joints (septic arthritis) and bones (osteomyelitis)
Staphylococcus aureus
endocarditis
infection on the valves of the heart
forms biofilm on the heart valve
difficult to treat, frequently leads to death
especially common in intravenous drug users
Staphylococcus aureus
clinical signs of endocarditis
Osler’s nodes, Janeway lesions, conjunctival hemorrhages, and heart murmurs
Toxic Shock Syndrome (TSS)
symptoms include high fever, vomiting, diarrhea, sore throat, muscle pain, rash, hypotension or shock, organ failure
desquamation of the skin occurs upon resolution
associated with tampon use -> colonizes the vagina -> produce TSST-1
wound infections can also lead to TSS, but usually associated with enterotoxins
Staphylococcus aureus
Staphylococcal food poisoning
self-limited episode of vomiting and diarrhea
begins 2-5 horus after ingestion of food contaminated with enterotoxins
Staphylococcus aureus
scalded skin syndrome
characterized by desquamation
usually in infants and children under the age of 5
results from exfoliatin secretion
usually localized but if toxin reaches the bloodstream, can see exfoliation at remote sites
Staphylococcus aureus
nosocomial infections
infections that are acquired after people are admitted to the hospital and have undergone procedures such as mechanical ventilation, surgery, or catheter placement
Staphylococcus aureus
leading cause
Staphylococcus aureus diagnostic laboratory tests
Gram-stain of tissue specimens - gram-positive cocci
culture on blood agar plates - colonies will have gold color
catalase-positive
coagulase-positive (S. epidermidis and S. saprophyticus are coagulase-negative)
treatment of Staphylococcus aureus
drainage of collections of pus
penicillin, now almost all produce beta-lactamase
antistaphylococcal penicillins such as methicillin, nafcillin, oxacillin
cephalosporins such as cefazolin and cefuroxime
MRSA
methicillin-resitant Staphylococcus aureus
widely found in hosptials
contain a variant penicillin-binding protein called PBP2’
does not bind most beta-lactam antibitics
encoded by mecA gene
treat with vancomycin, linezolid, daptomycin, or quinupristin/dalfopristin
CA-MRSA
community-acquired MRSA
common and genetically distinct from most hospital-acquired MRSA
produce PVL toxin
may be associated with mroe severe infections
Staphylococcus aureus
treatment of S. epidermidis
most isolates are resistant to antistaphylococcal penicillins and cephalosporins
referred to as MRSE (methicillin-resistant S.epidermidis)
treated with the same agents that are effective against MRSA
Streptococci
gram-positive cocci
catalase-negative
categorized by hemolysis
not strict anaerobes because can use catalase in medium such as blood
three types of streptococci hemolysis
alpha-hemolysis
beta-hemolysis
gamma-hemolysis
alpha-hemolysis
partial hemolysis with greenish tint, includes the viridans streptococci and Streptococcus pneumoniae
beta-hemolysis
complete, clear hemolysis
includes most of the “groubable” streptococci such as S. pyogenes, S. agalactiae, and several other species
gamma-hemolysis
a misnomer - no memolysis
includes S. bovis and many of the enterococci
Viridans streptococci
alpha-hemolytic
more than 20 species, generally nongroupable
some colonize oropharynx and cause dental caries or bacterial endocarditis following transient bacteremia
others are associated with deep tissue abscess formation
Streptococcus pneumoniae
alpha-hemolytic stretococci
leading cause of community-acquired pneumonia
beta-hemolytic streptococci
often broken down as “groups” based on surface carbohydrates
Group A - S. pyogenes
Group B - S. agalactiae
Group D - S. bovis and enterococci
Streptococcus pyogenes
Extracellular pathogen
called “pyogenic” because it causes purulent (lots of pus) infections
also referred to as “group A streptococci”
gram-positive cocci in chains
streptolysin
two types - streptolysin O (SLO) and streptolysin S (SLS)
SLO forms pores in the plasma membranes of human cells
responsible for the beta-hemolysis seen on blood agar
diagnosis through ASO titers
Streptococcus pyogenes
M-proteins
fibrillar molecules that extend out beyond the surface of the bacterium
anchored in the peptidoglycan
used to serotype S. pyogenes
prevent phagocytosis
Streptococcus pyogenes
Streptococcal pyrogenic exotoxins (SPEs)
also called “erythrogenic toxins”, “scarlet fever toxins”
3 major types (SPE A, B, and C)
rash of sarlet fever, may play a role in stretococcal toxic shock syndrome
share sequence homology and biological activity with some of the Staphylococcus aureus enterotoxins
superantigens (except for SPE B) - may contribute to hypotension and shock
SPE A and SPE C are carried by phage
SPE B is a protease - may contribute to tissue destruction in necrotizing fasciitis
Streptococcus pyogenes
streptokinase
causes lysis of fibrin clots by converting plasminogen to plasmin
used to lyse artery clots in patients with acute myocardial infarctions
Streptococcus pyogenes
C5a peptidase
extracellular enzyme that cleaves the complement component C5a
prevents the recruitment of phagocytes to sites where bacteria are
Streptococcus pyogenes
clinical disease caused by Streptococcus pyogenes
streptococcal pharyngitis
scarlet fever
streptococcal toxic shock syndrome
impetigo
cellulitis
necrotizing fasciitis
nonsuppurative sequelae
clinical disease of Staphylococcal aureus
furuncles and carbuncles
joint and bone infections
endocarditis
toxic shock syndrome
staphylococcal food poisoning
scalded skin syndrome
cellulitis
hospital-acquired infections
determinants of pathogenicity for Staphylococcus aureus
toxic shock syndrome toxin 1
staphylococcal enterotoxins A-E, G-I
exfoliatin
alpha-toxin
PVL
coagulase
protein A
Determinants of pathogenicity for Streptococcal pyogenes
streptolysin
M-protein
streptococcal pyrogenic exotoxins
streptokinase
C5a peptidase
streptococcal pharyngitis
common, especially in children
sore throat, fever, headache, swollen erythematous tonsils, sometimes with puruelent xudates, cervical lymphadenopathy
self-limiting
impossible to clinically differentiate from viral pharyngitis
suppurative complications - peritonsillar and retropharyngeal abscesses
non-suppurative sequellae - rheumatic fever and post-stretpococcal glomerulonephritis
Streptococcus pyogenes
Streptococcal scarlet fever
an erythematous, “sand-paper” rash that may accompany streptococal pharyngitis
usually involves the face but spares the area around the mouth (circumoral pallor)
rash is accentuated in skin areas
strawberry tongue
Streptococcus pyogenes
Streptococcal Toxic Shock Syndrome
similar to the staph one except rash is rarely present and not associated with tampon use
fever, hypotension, and multi-organ failure
majority of patients are bacteremic and have associated soft-tissue infection
Streptococcus pyogenes
impetigo
infection of the epidermis
usually in small children
begins as small vesicles on exposed areas of the skin -> vesicles enlarge -> become pustular -> rupture to form a yellow crust
Streptococcus pyogenes
cellulitis
deeper form of skin infection
involves dermis and subcutaneous tissues
associated with fever and lymphangitis
often located at anatomic sites with compromised lymphatic drainage
special form of group A streptococcal cellulitis: erysipelas - indurated, erythematous rash, well cemarcated, rapidly enlarging, usually on the face
Streptococcus pyogenes
necrotizing fasciitis
involves deeper tissues, including the superifical and/or deep fascia of the muscles - life-threatening
source of infection may be a minor break in the skin or a surgical wound
abrupt onset - severe pain at site of infection, fever, malaise, only minimal physical findings
tissue damage progresses rapidly
skin becomes mottled and dusky as the underlying tissues become necrotic
bullae may develop on the surface of the skin
Streptococcus pyogenes
acute rheumatic fever
acute rheumatic fever
thought to be an autoimmune disease following S. pyogenes infections
most notable for permanently damaging the valves of the heart
begins 3 weeks after onset of pharyngitis
does not follow soft-tissue infections
JONES criteria
Streptococcal pyogenes
Jones criteria
for diagnosis of acute rheumatic fever
major criteria - polyarthritis (J), carditis (O - heart), subcutaneous nodules (N), erythema marginatum (E), sydenham chorea (S)
minor criteria - arthralgia, fever, elevated sedimentation rate of C-reactive protein, prolonged PR-interval on EKG
must have 2 major or 1 major and 2 minor criteria
must also have evidence of a recent group A streptococcal infection
Streptococcal pyogenes
poststreptococcal glumerulonephritis
characterized by edema, hypertension, hematuria, and proteinuria
follows infection with either respiratory or skin strains
usually self-limited
Streptococcal pyogenes
diagnostic laboratory tests for Streptococcal pyogenes
gram-stain of tissue specimens - gram-positive cocci in chains
culturable on blood agar plates - causes beta-hemolysis and are catalase-negative
rapid strep tests are used to diagnose pharyngitis
anti-streptolysin-O antibody titers
treatment for Streptococcal pyogenes
penicillin is the treatment of choice
macrolides are alternatives
some reccomend that severe infections should be treated with penicillin plus clindamycin because clindamycin inhibits the production of SPEs, which may play a role in these diseases
immediate surgical debridement in necrotizing fasciitis
intravenous immunoglobin in STSS - contains antibodies against streptococcal toxins
prevention of Streptococcal pyogenes
no vaccines currently available
penicillin prophylaxis is used to prevent recurrence of rheumatic fever during most susceptible ages
Streptococcus agalactiae
also referred to as “group B stretococci”
causes neonatal sepsis and neonatal meningitis
normally colonize the vagina -? passed to the newborn during delivery
pregnant women who screen positive for GBS are often treated with penicillin G or vancomycin before delivery to prevent infection of newborn
Streptococcus bovis
a member of the group D streptococci (gamma-hemolytic)
not enterococci
rarely cause infections
blood infections due to this bacterium are associated with gasto
enterococci
formerly classified as group D streptococci
reclassified as a separate genus based upon biochemical and growth characteristics
normal inhabitants of the gastrointestinal tract
species of medical significance are E. faecalis and E. faecium
E. faecium tends to be more resistant to antimicrobials, whereas E. faecalis is mroe common
Enterococci determinants of pathogenicity
low intrinsic virulence
vancomycin-resistant enterococci or VRE
VanA operon - part of a transposon, transposon carried by a self-transferable plasmid, allows for the synthesis and substitution of D-Ala-D-lactate for D-Ala-D-Ala, so vancomycin cannot bind
clinical disease of enterococci
common cause of hospital-acquired infections
urinary tract, wounds, biliary tract, intra-abdominal infections
bacteremia - intravascular catheters and endocarditis
Enterococci diagnostic laboratory tests
easily grown on blood agar - gamma-hemolysis and occassionally beta or alpha-hemolysis
grow int he presence of high concentrations of bile salts and sodium chloride
treatment of enterococci
antibiotic resistance is especially problematic
penicillin or ampicillin are bacteriostatis against enterococci
add aminoglycosides for bactericidal activity
significant reistance to vancomycin
linezolid, quinupristin/dalfopristin, or daptomycin
overuse of vancomycin predisposes to VRE colonization/infection
prevention of Enterococci
hand-washing and contact precautions are important in limiting the spread of VRE
judicious use of vancomycin
gram-positive rods
- Listeria monocytogenes*
- Corynebacterium diphtheriae*
- Bacillus anthracis*
Bacillus
aerobic gram-positive rods
two are of medical importance:
- Bacillus anthracis, which causes antrhax
- Bacillus cereus, which causes food-poisoning
Bacillus anthracis
grow in chains (bamboo rods)
spore-forming, spores are resistant to dry heat and some disinfectants - may persist in dry earth for years
historically, a major agricultural problem, infected animals die and return a high load of spores back to the soil, where they can later infect other animals
Bacillus anthracis determinants of pathogenicity
virulence factors carried on plasmids
anthrax toxin
capsule
Bacillus anthracis capsule
composed of D-glutamic acid encoded on pXO2 plasmid
antiphagocytic properties
anthrax toxin
an A-B toxin, encoded on a plasmid
A (activity) subunit and B(binding) subunit
A = elongation factoer (EL) and lethal factor (LF)
B = protective antigen (PA)
PA binds to cells and facilitates the entry of EF and LF
EF has adenylate cyclase activity and leads to edema and inhibition of neutrophil function - increases cAMP
LF is a zinc protease, cleaves host cell kinase and leads to macrophage cell death
Bacillus anthracis
cutaneous anthrax
spores are introduced into the skin
small red macule appears
enlarges to form an ulcer
blackened necrotic eschar
expanding zone of edema
painless
surrounded by small satellite vesicles
ususally spontaneously resolve
inhalation anthrax
spores are inhaled, often following hte handling of contaminated hides, hair, or wool
symptoms similar to those of a severe viral respiratory infection - fever, shortness-of-breath, and hypotension
death results
large necrotic hemorrhagic mediastinal lymph nodes are common
organisms sometimes seen on peripheral blood smears
Bacillus anthracis
gastrointestinal anthrax
ulcers form at site of infection after ingestion of contaminated mean
disease is rare in humans
the GI tract is the common route of infection in herbivores
mortality rates between those of cutaneous and inhalation anthrax
Bacillus anthracis
diagnostic laboratory tests for Bacillus anthracis
large numbers of organisms can be seen by Gram-stain of cutaneous lesions
between 10^7 and 10^8 bacteria/mL can be seen in the blood in late-stage disease
the bacterium will also grow from pus or sputum streaked onto blood agar plates
serologic tests are available
Bacillus anthracis
treatment of Bacillus anthracis
penicillin
because of concerns regarding weaponized strains, now ciprofloxacin and doxycycline are recommended
for inhalational anthrax, add a second agent, such as rifampin, vancomycin, penicillin, clarithromycin
prevention of Bacillus anthracis
a nonliving vaccine with PA as its active component is used in humans
recommended for certain agricultural workers, veterinary perosnnel and others at risk for exposure to anthrax
a live attenuated vaccine containing spores is used in domestic animals
post-exposure prophylaxis - ciprofloxacin for 60 days for presumed exposure to control
listeria
only one species
Listeria monocytogenes - of signiciant medical importance
Listeria monocytogenes
metabolically facultative
grows well at refrigeration temperatures
infects many animals, causes curling disease adn stillbrith in sheep and cattle
foodborne transmission - through unpateurized milk, hceestek
Listeria monocytogenes determinants of pathogenicity
facultative intracellular pathogen
internalin
listeriolysin O
ActA
facultative intracellular pathogen
can grow and replicate in teh environment
the ability to invade eukaryotic cells is an essential step in pathogenesis
other facultative intracellular pathogens include Salmonella, Shigella, Legionella, and Mycobacteria
Listeria monocytogenes
internalin
mediates attachment of and invasion of mammalian cells
factors that mediate adherence of bacteria to eukaryotic cells are called adhesins
Listeria monocytogenes
listeriolysin O
a pore-forming toxin
initially, bacteria reside inside the vacuoles
quickly escape via the action of this protein
Listeria monocytogenes
ActA
bacterial protein that help bactera propel themselves around the cytoplasm
forms and pushes against actin tails
helps form protrusions into neighboring epithelial cells
membranes surrounding this protrusions are lysed
bacteria enter the cytoplasm of the adjacent cell
net result - spread without exposure to the external environment (or the humoral immune system)
Listeria monocytogenes
clinical disease of Listeria monocytogenes
meningitis - elderly, young, immunocompromised (rarely associated with a monocystosis)
fetal infections - premature labor and intrauterine fetal demise
causes neonatal infections such as sepsis, respiratory distress, and disseminated abscesses
diagnostic laboratory tests for Listeria monocytogenes
growth of the organism from cerebral spinal fluid, blood, or amniotic fluid
small, smooth colonies surrounded by a narrow rim of beta-hemolysis when grown in blood agar plates
catalase positive
treatment of Listeria monocytogenes
ampicillin is the treatment of hoice - may be used in combination with an aminoglycoside
trimethoprim-sulfamethoxazole - alternative
prevention of Listeria monocytogenes
avoid raw meat and unpasteurized milk
thoroughly wash raw vegetables
Corynebacteria
aerobic Gram-positive bacilli
irregular swelling on one end - “club shape”
Corynebacterium diphtheriae causes diphtheria
other corynebacterium species are normal inhabitants of the skin
Corynebacterium diphtheriae
nonspore-forming
infects only humans
Diphtheria toxin (DT)
gene carried on phage, A-B toxin
fragment A inhibits peptide chain elongation by ADP-ribosylating EF-2
inhibits protein synthesis in pharyngeal epithelial cells, leading to necrosis -> pseudomembrane formation
ADP-ribosylating toxins transfer ADP-ribose from NAD to host cell proteins -> alters the activity of these proteins
Corynebacterium diphtheriae
ADP-ribosylating toxins
exotoxin A of Pseudomonas aeruginosa
cholera toxin of Vibrio cholerae
heat labile toxin of Exherichia coli
pertussis ctoxin of Bordetella pertussis
diphtheria toxin of Corynebacterium diphtheriae
clinical disease of Corynebacterium diphtheriae
diphtheria:
- person-to-person spread by direct contact or droplets
- sore throat, fever, difficulty swalling, cough, hoarseness, and rinorrhea
- pseudomembrane on oropharnx, palate, nasopharynx, nose, or larynx
- composed of necrotic cell debris, fibrin, and blood cells
- may lead to airway obstruction
- DT may be absorbed into the circulation and lead to distant tissue damage
- dmage to the heart -> cardiac arrhthmias
- nerve damage -> paralysis of eye muscles, soft palate, and extremities
- adrenal damage may lead to hypoadrenalism
diagnostic laboratory tests for Corynebacterium diphtheriae
in stained smears, bacteria lie in clusters at acute angles to each other (“Chinese letter” appearance) or in parallel groups (“palisade” appearance)
tellurite selective medium -> black colony with a surrounding gray-brown halo
all isolates should be checked for DT production through PCR, antisera reactivity, or biological activity in tissue culture or guinea pigs
treatment of Corynebacterium diphtheriae
horst antisera against DT
antibiotics do not increase the rate of healing in people who have received antitoxin, but they are given to prevent spread of the organism
macrolides, penicillin G, rifampin, and clindamycin
monitored closely for respiratory or cardiac failure
close contacts should be cultured and given a vaccination booster if required
prevention of Corynebacterium diphtheriae
diphtheria toxin vaccine - treatment of DT with formaldehyde
a toxoid is a chemically treated toxin that is no longer toxic but retains immunogenicity
diphtheria toxoid vaccine has led to a dramatic reduction in cases of diphteria in the US
vaccinated individuals, although protected from disease, may still be colonized
anaerobes and related bacteria
- Clostridium* spp.
- Actinomyces israelii*
- Nocardia* spp. (not an anaerobe but closely related)
- Peptostreptococcus* spp.
Clostridia
Clostridium tetani, C. botulinum, C. perfirngens, and C. difficile
each is associated with its own characteristic medical manifestations
Gram-positive anaerobic rods, spore-forming
Clostridium tetani
cause of tetanus
found in soil and animal feces
spores remain viable in soil for many years
Clostridium tetani determinants of pathogenicity
Tetanus toxin
tetanus toxin
an A-B toxin
blocks the release of inhibitory neurotransmitters
homologous to botulnum toxin
Clostridium tetani
clinical disease of Clostridium tetani
cause of tetanus
follows inoculation of wounds with spores
germination of spores occurs in low oxidation-reduction potential environments such as wounds with devitalized tissue or foreign bodies
toxin produced and binds to peripheral motor neuron terminals
enters axons and is transported to neuron cell bodies in the central nervous system by intra-axonal retrograde transport
toxin blocks the release of presynaptic inhibitory neurotransmitters
net effect is the INCREASE in the resting firing rate of motor neurons, leads to muscle rigidity
symptoms include lockjaw, increased tone of neck, shoulder, and back muscles, and eventually the abdominal and leg muscles
spasms - invoked by minor stimuli, may compromise respiration - sympathetic nervous system affected
leads to hypertension, tachycardia, arrhythmia, sweating, vasoconstriction
neonatal tetanus - infection of umbilical stump
diagnostic laboratory tests for Clostridium tetani
isolation of organism from woudns not helpful
terminal spores are tennis racket or durmstick shaped
demonstration of tetanus toixn production is necessary for definitive identification of the organism
treatment of Clostridium tetani
penicillin or metronidazole, although unproven value
human tetanus immunoglobulin
agents to control muscle spasms
prevention of Clostridium tetani
vaccine - tetanus toxoid
Clostidium botulinum
cause of botulism
subterminal spores
naturally found in soil, pinds, lakes, and on plants
bees collect C. botulinum spores along with pollen from flowers, resulting in high concentrations of these spores in honey
biological warfare concern - “weaponized” toxin developed that can be absorbed through skin
*Clostidium botulinum *determinants of pathogenicity
botulinum toxin and some varients encoded by bacteriophages
associates with home-canned food products - spores survive the canning process and germinate in the anaerobic environment of the sealed food containter
toxin is secreted and not destroyed if the food is not reheated (destroyed if boil for 10-15 minutes)
food is ingested, toxin enters bloodstream, reaches cholinergic terminals at perpheral motor endplates, cleaves components of neuroexocytosis apparatus and blocks release of acetylcholine
blocks transmission of nerve impulses and the net effect is DECREASED motor neuron activity
botulinum toxin
homologous to tetanus toxin
A-B toxin
protease
one of the most potent toxins known
some variants are encoded by bacteriophages
Clostidium botulinum
three types of botulsim
food-borne botulism
wound botulism
infant botulism
Clostidium botulinum
food-borne botulism
ingested toxin leads to:
symmetric descending paralysis
cranial nerve involvement - diplopia, dysarthria, dysphagia, respiratory failure
nausea, vomiting, and abdominal pain
fever is unusual
Clostidium botulinum
wound botulism
occurs when a wound is contaminated with C. botulinum spores
symptoms are similar too food-borne botulism but no GI findings
Clostidium botulinum
infant botulism
C. botulinum colonizes the infant intestine
toxin produced and absorbed
paralysis
infants less than 6 months of age are particularly susceptible because they lack normal flora
no honey to infants less than 12 months of age
Clostidium botulinum
Clostidium botulinum diagnostic laboratory tests
compatible history and clinical symptoms
isolation of toxin or the organism
ocasionally, toxin can be isolated from the blood of patients
treatment of Clostidium botulinum
respiratory support
trivalent equine antitoxine
antibiotics to eliminate residual bacteria from the bowel are of unproven efficacy
prevention of Clostidium botulinum
no vaccine is available
proper canning techniques
Clostridium perfringens
causes food-poisoning
associated with ingestion of contaminated meat, poultry, or vegetables
also causes gangrene
Clostridium difficile
causes diarrhea associated with antibiotic use
Actinomycetes
true bacteria that resemble funcgi
related to the mycobacteria - some members are partially acid-fast
medically important - Nocardia spp., Actinomyces spp.
note that Nocardia are aerobic
medically important Nocardia spp.
- N. farcinica*
- N. asteroides*
- N. brasilliensis*
Norcadia spp.
gram-positive bacilli, aerobic
cells remain together after division and form elongated chains or filaments with occasional branches
branched filaments irregularly take up gram stain and have “beaded” appearance
common inhabitants of the soil
Nocardia spp. determinants of pathogenicity
neutralize oxidants, prevent phagosome acidification, and inhibit phagosome-lysosome fusion
lesions ar extensively infiltrated with neutrophils, but bacteria not killed
cell-mediated immunity is needed to control the infection
Nocardia spp. clinical disease
infects individuals with deficient cell-mediated immunity
pulmonary nocardiosis - causes subacute pneumonia, nodules, cavitation, and empyema, dissemination to the central nervous system, skin, and soft tissue, and other organs, dissemination leads to abscess formation
transcutaneous inoculation - inoculation of the organism into the tissues of the foot, fistula formation, discharge of serous or purulent material containing small “sulfur” granules
lesions spread slowly to involve skin, subcutaneous tissue, and bone
Nocardia spp. diagnostic laboratory tests
gram staining of lesion speciments (filaments with beaded appearance)
routine laboratory media such as blood agar plates
requires 2 weeks to grow
will partially stain using acid-fast technique
Nocardia spp. treatment
trimethoprim/sulfamethoxazole and other sulfa drugs
minocycline and amikacin are alternatives
prone to relapse, so treatment is often continued for 6 to 12 months
drainage of brain abscesses and debridement of actinomycetomas
Nocardia spp. prevention
no vaccine is currently available
Actinomyces israelii
gram-positive bacilli
non-spore-forming
similar to Nocardia spp. except anaerobic
normal flora, found in the mouth and gastrointestinal tract and female genital tract
Actinomyces israelii determinants of pathogenicity
iundolent, suppurative infections with fistulas and sulfur granules
infected foci spread contiguously, ignoring tissue planes
Actinomyces israelii clinical disease
poor dentition or trauma leads to oral-cervicofacial disease
aspiration of mouth contents leads to involvement of the pulmonary parenchyma and pleural space
infection may spread and involve bone and chest wall
often mistaken for malignancy
abdominal or pelvic disease may follow intestinal rupture or UID use
Actinomyces israelii diagnostic laboratory tests
gram-stained sulfur granules
growth of the organism from culture of these specimens
in the absence of sulfur granules, it is difficult to determine if the organism is causing disease
not particularly acid fast
Actinomyces israelii treatment
penicillin
prolonged treatment regimens - up to 12 months
tetracycline/doxycycline is used in penicillin allergic patients
Actinomyces israelii prevention
no vaccine is currently available
