features of bacterial infection are:
Types of shock you can encounter with infection
Toxic shock: She has the classical constellation of toxic shock syndrome characterized by
Toxic shock syndrome is caused by strains of
S. aureus can be normal vaginal flora in 8-10% of females, although heavy vaginal growth of S. aureus is unusual.
Pathophysiology of Toxic shock syndrome
TSST-1 is a true exotoxin because it is secreted during cell growth rather than after cell lysis.
This toxin is a super antigen which activates T cells by binding antigen-presenting cells to the V$ chains of the T-cell receptor.
Super antigens can activate 5-25 % of the total T-cell population rather that 1-2% activated by the more physiological mechanism of processed antigen causing excessive release of cytokines (IL-2, TNF), that leads to many signs and symptoms of the illness.
In order to prove this isolate is the etiologic agent of toxic shock syndrome, it should be demonstrated that the isolate produced Toxic Shock Syndrome Toxin-1 (TSST-1).
One of the key observations in the initial epidemic of TSS was that the disease was most severe in women who used super absorbent tampons.
It is known that TSST-1 is produced under conditions of low magnesium ion concentration.
It is speculated that the tampons act to absorb various ions including magnesium, providing optimal conditions for production of TSST-1.
These strains are found in surgically related infections and at other body sites.
A similar type of illness is also caused by Streptococcus pyogenes, which produces streptococcal pyrogenic exotoxins SPE A, B. or C.
Therapy consists of fluid and electrolyte replacement and identification and drainage of any focally infected site, such as an abscess. Antibiotic therapy should be based on the susceptibility pattern of the isolate. The following antibiotics can be used
Mthicillin resistant Staph aureus
Clinical presentations of S. aureus infection
Both Staphylococcus aureus and Streptococcus pyogenes (group A strep) have many enzymes which act as virulence factors allowing these bacteria to invade tissue from patients with normal immunity and spread from infection at a local site to the bloodstream.
Common causes for Pharyngitis are:
Throat culture four weeks after Pharyngitis and following Amoxacillin is most likely to be negative.
It should be noted that viral pharyngitis occurs at least as frequently as strep pharyngitis, therefore, a rapid test antigen screen (45 minutes) for Streptococcus pyogenes or a culture (48 hours) is used to establish the diagnosis (catalase negative colonies which are beta hemolytic).
Rheumatic fever is a reasonable choice because of
Rheumatic fever occurs in about 3% of times following Streptococcal pharyngitis.
Rheumatic fever is a non-suppurative sequela of Streptococcus pyogenes infections.
It occurs approximately 3 weeks after streptococcal pharyngitis.
By the time the symptoms are apparent, the throat culture is negative. A recent history of streptococcal pharyngitis supports the diagnosis of rheumatic fever.
Rheumatic fever is characterized by
Sub Q nodules
Colonies of Streptococcus pyogenes are beta hemolytic due to two distinct hemolysins: streptolysin S and streptolysin O.
The beta hemolytic streptococci are classified into Lancefield groups based on unique carbohydrate antigens in their cell wall. Streptococcus pyogenes is designated as Lancefield group A.
Unlike streptolysin S. streptolysin O is oxygen labile. Throat cultures must be incubated anaerobically or the blood agar plates must be stabbed to demonstrate the potent hemolysin, streptolysin O (Cytotoxin, lyses RBC's and WBC's).
Patients with RF will frequently mount (80%) a humoral immune response to streptolysin O.
The test used to measure antibodies against this hemolysin is called an ASO (anti-streptolysin O) titer. An elevated ASO titer in individuals with appropriate clinical symptoms supports the diagnosis of RF, when culture results are negative.
Pathogenesis of rheumatic fever
M protein is an important virulence factor found in the cell wall (Pili) of Streptococcus pyogenes.
M protein has been found to be antiphagocytic and it also has epitopes which are antigenically similar to one found in the cardiac myosin and sarcolemmal membrane proteins.
Acute RF is thought to be an auto-immune disease. Antibodies directed against M protein cross-react with cardiac tissue. These antibodies bind to the cross-reactive antigens in muscle and damage the muscle tissue. Other group A strep antigens may also cross-react with other cardiac antigens causing damage to the heart valves.
Acute : Causes Pancarditis (Pericardium, Myocardium and endocardium)
Chronic: Progressive valvular fibrosis with thickening and sclerosis of valves, adhesion of commisures, thickening, shortening and adhesions of chordee, calcification.
Other virulence factors of Streptococcus pyogenes
Additional virulence factors of S. pyogenes include These enzymes help spread infection further into tissue.
Streptokinase : Lyses fibrin
Clinical presentations of group A streptococcal infection
Pharyngitis: Sorethroat, fever, cervical lymphadenopathy, swollen red tonsils with white or yellow patches
Rheumatic fever: Auto-immune process. Systemic inflammation affecting Heart, Joints and Skin.
Acute Glomerulonephritis: Auto-immune process.
Toxic shock syndrome: Pyrogenic exotoxins A,B or C. Stimulates T cells to release of Cytokines. Shock and failure of multiple organs. Superantigens
Scarlet fever is a manifestation of group A streptococcal pharyngitis in which the infecting strain produces a specific virulence factor called erythrogenic toxin, which is coded for by a phage.
Production of this toxin is manifested clinically by the appearance of a scarlatinal (bright red) rash beginning on the chest and spreading to the trunk and neck, then to the extremities. The rash is not seen on the face, or the palms or soles.
A "strawberry" tongue is frequently seen with this disease as well.
Rheumatic fever can be a post-streptococcal sequela of scarlet fever just as it may be follow strep throat caused by strains which do not produce erythrogenic toxin.
Necrotizing Fascitis: Bacterial infection of fibrous tissue thatt covers the body beneath the skin. "Flesh eating bacteria" . Significant mortality.
Penicillin for 10 days to prevent recurrence or complications
Symtomatic therapy (Tylenol, Fluids and electrolytes)
Complications ( Acute glomerulonephritis, Carditis etc)
Surgical debridement: in Necrotizing fascitis
Normal intact endothelium resists implantation by organisms. Very virulanr pathogens may be able to cause endovascular infection. Acute infective endocarditis.
Sub acute infective endocarditis: If there is damaged valves the organisms can implant on them. Endothelial injury inflicted by the organisms release tissue factors to activate platelets and fibrin-platelet vegetaions ( clot ) forms. These start off as non-bacterial thrombotic endocarditis (NBTE). Organisms of low virulence colonize these NBTE and cause endovascular infection.
Signs and symptoms
The manifestations of infective endocarditis are protean since any organ can be involved.
Infective: Fever, Weight loss, anorexia, malaise, splenomegaly, leucocytosis
Vegetations: New murmurs, destruction of valve leading to insufficiency followed by hear failure
Janeway lesions (erythematous macules and papules on the palms and sole)
Osler nodes (tender raised erythematous lesions on the finger and toe pads )
Splinter hemorrhage in the nail beds
Roth spots (Petechiae in retina with white centers)
An echocardiogram revealed vegetations on her aortic valve.
The Gram stain is suggestive of a streptococcus since cocci in chains were observed.
This is verified by the negative catalase which separates the streptococci from the staphylococci.
Additional biochemical reactions of a positive bile esculin hydrolysis and PYR (pyrrolidonyl-beta-naphthyl amidase) hydrolysis are indicative of an enterococcus.
The species cannot be given based on this data. A more complete battery of biochemical testing is required to further identify which species of enterococcus was isolated.
E. faecalis is the most common species in clinical infections (85%); E. faecium is second (12%), the remaining isolates are a variety of Enterococcus species.
Failure to improve on antibiotics
Because this organism is not susceptible to vancomycin and ampicillin, there is no adequate antibiotic therapy reaching the infection.
The organism is labeled a VRE (vancomycin resistant enterococcus).
Most likely the organism is E. faecium, which is intrinsically resistant to ampicillin and has acquired a gene to change its cell wall composition so that vancomycin can not disrupt cell wall synthesis and inhibit the growth of the bacteria.
In addition the orgnims are inside avascular vegetations, Antibiotis and Phagocytes do not have easy access. They are also in lower metabloic state.
The enterococci also require a breakdown of host's defenses or mucosal barriers to cause infection.
Her an A-V fistula broke down the barrier of the skin and mucous membranes and serves as a conduit for microorganisms to travel from the superficial sites into the bloodstream.
The enterococci do not have M protein, hemolysins, or toxins which act as virulence factors for the beta hemolytic streptococci.
Other infections are commonly caused by this group of organisms
Usually enterococci are associated with urinary tract infections and mixed bacterial wound infections, such as decubiti. They cause sepsis and rarely meningitis.
The enterococci are normal flora of the gastrointestinal tract and are present in the gastrointestinal tract of animals and on plants. They lack the virulence factors of the staphylococci and beta hemolytic streptococci, but are significant pathogens because of their intrinsic antimicrobial resistance.
Any patient whose cultures have VRE must be placed on barrier precautions, which entails gloves and gown for anyone handling the patient or objects in their environment.
A mask is not required.
When a patient has VRE, most likely they are carrying the organism in their GI tract. Items in their room readily become colonized so that VRE can be isolated from bed rails, call buttons, etc.
Hand washing is an important means by which the transmission of VRE can be reduced.
S. epidermidis, require a breakdown of the host's skin or mucosal barriers to cause infection.
The introduction of central lines, venous catheters, or prosthetic devices provide an entrance route to the body for this organism that does not produce the virulence factors that more pathogenic organisms do.
Once the barrier has been compromised, S. epidermidis may produce "slime", a biofilm that aids in the adherence of the bacteria to the synthetic surface of the device and protects the bacteria from phagocytosis and antimicrobials.
Antimicrobial therapy may eliminate the organisms from the blood stream.
But persistent bacteremia indicates that the catheter must be removed for eradication of the infection.
Coagulase negative staphylococci are usually resistant to oxacillin, nafcillin, and methicillin. If the isolate is methicillin resistant, treatment with the first generation cephalosporins is not effective. Vancomycin is usually the drug of choice for methicillin resistant staph infections.
Access to humans
S. epidermidis and other coagulase negative species of staphylococci are normal commensals of the skin, anterior nares, and external ears in humans and animals.
These organisms may contaminate prosthetic devices
joint replacements) during implantation or post-surgical manipulation.
Neonates and neutropenic patients are particularly at risk.
Because coagulase negative staphylococci are present on the skin, identification of staphylococci in blood cultures may represent either contamination or a clinically significant finding. Distinguishing between the two is often difficult.