5.3 Endocarditis, Bone Marrow Pathogens, and Pathogenicity

5.3 Endocarditis, Bone Marrow Pathogens, and Pathogenicity

Quick Answer: Endocarditis agents are viridans-group streptococci, S. aureus, Enterococcus, CoNS on prosthetic valves, and HACEK (Haemophilus/ Aggregatibacter, A. actinomycetemcomitans, Cardiobacterium, Eikenella, Kingella). Bone-marrow agents to memorize are Brucella and Salmonella. Virulence that the exam names: protein A, coagulase, pneumococcal capsule, endotoxin, and catheter biofilm. Work Brucella in a BSC; do not sniff plates.

Outline II.A finishes with three linked ideas: which organisms stick to heart valves, which organisms hide in bone marrow, and which virulence tricks explain those tropisms. This is still Bacteriology (45–55% of M). If section 5.1 was the instrument and 5.2 was the colony, this section is why the bottle mattered and how the organism hurts the patient. Keep /practice/ascp-m nearby for items that mix a valve history with a fastidious Gram-negative rod.

Common agents of endocarditis

Infective endocarditis is infection of the endocardial surface, usually a valve leaflet, a chord, or prosthetic material. Organisms arrive by continuous or recurrent bacteremia and then adhere. That is why blood cultures in suspected endocarditis are multiple sets over time, not a single through-line draw, and why a true pathogen often flags in all sets with a short time to positivity.

Viridans-group streptococci (S. sanguinis, S. mitis group, S. mutans, S. salivarius, and the S. anginosus group) are the classic subacute native-valve organisms. They live in the mouth, seed damaged valves after dental bacteremia, and make dextran or similar adhesins that stick to fibrin-platelet vegetations. The anginosus (milleri) group is the viridans cluster more associated with abscesses than with textbook subacute endocarditis, but it still appears in blood. On the bench they are alpha-hemolytic, optochin resistant, and bile insoluble—the distinction you already use versus S. pneumoniae. S. pneumoniae itself can cause acute destructive endocarditis, but it is not the “viridans subacute” story.

Staphylococcus aureus causes acute endocarditis on previously normal or damaged valves and is the leading organism in injection-drug use (often right-sided/tricuspid). It is also a major prosthetic-valve pathogen. A single positive bottle is enough to start the workup; waiting for a second set because “staph might be a contaminant” is how S. aureus endocarditis is missed. S. lugdunensis belongs in this conversation even though it is coagulase negative: it behaves like S. aureus on native valves.

Enterococcus spp. (E. faecalis more than E. faecium in classic endocarditis) appear in older men with urinary or biliary sources and in younger women after obstetric procedures. They are hardy, they endure on damaged valves, and they force you to think about ampicillin plus an aminoglycoside or ampicillin plus ceftriaxone for synergy—AST details live in the susceptibility chapter, but the blood-culture bench is where the organism is first named.

Coagulase-negative staphylococci, especially S. epidermidis, are the signature organisms of prosthetic-valve endocarditis and pacemaker-lead infection. They arrive at surgery or via a line, then live in biofilm. Native-valve CoNS endocarditis happens, but on the exam a CoNS blood isolate plus a prosthetic valve is a pathogen until proven otherwise, whereas a CoNS isolate plus a structurally normal valve and one late bottle is still judged with the contaminant rules from section 5.2.

Other blood pathogens can land on valves—S. pneumoniae, beta-hemolytic streptococci, Candida (prosthetic valves, TPN, injection-drug use), and Gram-negative rods—but the outline’s “common agents” list you must be able to recite is viridans streptococci, S. aureus, Enterococcus, prosthetic CoNS, and HACEK.

HACEK organisms: fastidious, prolonged attention

HACEK is the mnemonic for a group of fastidious Gram-negative rods that cause subacute endocarditis, often on already abnormal valves, with a more indolent course than S. aureus:

• H — Haemophilus species now largely reassigned to Aggregatibacter (including A. aphrophilus, formerly H. aphrophilus / H. paraphrophilus)
• A — Aggregatibacter actinomycetemcomitans (formerly Actinobacillus)
• C — Cardiobacterium hominis
• E — Eikenella corrodens
• K — Kingella kingae

These organisms are capnophilic and fastidious. They grow poorly or not at all on MacConkey, prefer chocolate or blood agar in increased CO2, and may need the full routine blood-culture incubation—do not discard a clinically suspected endocarditis workup at 48 hours because the bottles are still negative. Modern continuous-monitoring media often recover HACEK within the standard 5-day protocol, which is why laboratories no longer routinely hold every bottle for 14 days, but the clinical history of culture-negative endocarditis still warrants a conversation with the physician about extended incubation, dedicated media, or 16S PCR on valve tissue.

Colony clues the exam likes: Eikenella may pit the agar and is classically associated with a bleach-like odor in bite-wound teaching—do not sniff unknown blood-culture plates to chase that odor. Kingella can pit as well and is a pediatric joint and endocarditis organism. Cardiobacterium may show rosettes on Gram stain. A. actinomycetemcomitans is a small coccobacillus linked to periodontal disease. None of these should go onto an open automated ID until Brucella/Francisella have been considered if the smear is a tiny GNCB and the growth is slow.

Culture-negative endocarditis (Coxiella, Bartonella, Tropheryma whipplei) is diagnosed by serology or PCR more than by the bacterial bottle; it is not a reason to skip drawing adequate-volume sets before antibiotics.

Agents of bone-marrow infection: Brucella and Salmonella

The outline’s named marrow pathogens are Brucella spp. and Salmonella spp. Marrow is cultured when blood is negative but intracellular or typhoidal infection is still likely, or when a hematology aspirate is inoculated because the clinician is already at the bedside.

Brucella (B. melitensis, B. abortus, B. suis, B. canis) is a tiny Gram-negative coccobacillus that lives inside macrophages. Transmission is zoonotic: livestock, veterinary work, and unpasteurized milk or cheese, not person-to-person droplets. Disease is undulant fever, night sweats, and often osteomyelitis or sacroiliitis; blood and bone-marrow cultures are both used because the organism’s density in blood may be low. On the plate it is slow, pinpoint, nonhemolytic, and usually does not grow on MacConkey. Oxidase and catalase are positive; urease is positive (B. suis can split urea rapidly). Work every suspected isolate in a biosafety cabinet. Do not sniff plates. Do not load an unresolved GNCB from blood or marrow onto an open automated identification instrument. Brucella is among the most notorious laboratory-acquired bacterial pathogens. Referral and select-agent paperwork belong to later chapters; the marrow bench’s job is not to aerosolize it.

Salmonella marrow infection is the typhoidal story. Salmonella Typhi (and Paratyphi) cause enteric fever; organisms seed the reticuloendothelial system. Bone-marrow culture remains positive later in disease—and after antibiotics—more often than blood culture, which is why the outline pairs Salmonella with marrow. Nontyphoidal Salmonella (S. Enteritidis, S. Typhimurium) cause gastroenteritis and can invade blood, especially in sickle cell disease, but the classic marrow teaching organism is typhoidal salmonellae. Colonies are Gram-negative rods, typically lactose negative on MacConkey, often H2S positive on TSI/HE (Typhi is a weak H2S producer with a characteristic TSI pattern), motile, and oxidase negative. They are not select agents, but they are reportable and they are true pathogens in blood or marrow.

Marrow may also grow mycobacteria, fungi, or Leishmania in the right host; those organisms are other outline sections. For II.A, do not leave an exam item about a livestock-exposed patient with a marrow GNCB, or a returning traveler with negative blood cultures and a request for marrow, without naming Brucella or Salmonella.

Organism pathogenicity: etiology, transmission, virulence

The outline’s pathogenicity bullet is not an invitation to recite every toxin in the textbook. It is a request for the mechanisms that explain bloodstream and endovascular disease.

Etiology and transmission first. Staphylococci and streptococci are usually endogenous: they leave the patient’s own skin, mucosa, or mouth and enter through a needle, a line, a dental extraction, or a break in the gut. S. aureus also spreads among people by contact. Enterobacterales and Candida translocate from gut or from a colonized catheter. Pseudomonas and A. baumannii are often exogenous hospital organisms on wet equipment and lines. Brucella is exogenous and zoonotic. Salmonella Typhi is fecal-oral, human reservoir; nontyphoidal salmonellae are foodborne zoonoses.

Virulence mechanisms the exam actually names:

• S. aureus protein A binds the Fc portion of IgG, flipping the antibody backward so complement and phagocytes cannot opsonize efficiently. Combined with coagulase, which converts fibrinogen to fibrin and walls the abscess or vegetation, protein A is why a Gram-positive cluster in blood is never “just another staph.”
• S. pneumoniae polysaccharide capsule is antiphagocytic. Encapsulated diplococci survive in blood and spinal fluid; unencapsulated laboratory strains look rough and are less virulent. Optochin and bile solubility identify the organism that carries that capsule. The same capsule chemistry is why bile lyses the cell wall and why a draughtsman colony appears as autolysis unmasks the center.
• Endotoxin (LPS) of Gram-negative organisms (Enterobacterales, Salmonella, and, with a different outer membrane, other GNR) triggers cytokine storm and septic shock when a bolus of organisms or free LPS hits the bloodstream. A rapidly flagging GNR bottle is a physiologic emergency, not only an identification exercise.
• Biofilm on catheters is how CoNS, S. aureus, Pseudomonas, and Candida turn a piece of plastic into a continuous source of bacteremia. S. epidermidis polysaccharide intercellular adhesin (PIA/ica) is the teaching slime. Biofilm explains differential TTP (high organism load in the through-line draw), why CoNS on a prosthetic valve are believed, and why pulling the line is source control rather than “more vancomycin forever.”

Put the pieces on one clinical line: a patient with a central catheter grows S. epidermidis from the through-line bottle 3 hours before the peripheral bottle because biofilm on the catheter dumped a high inoculum into the line draw. A patient with dental disease and a bicuspid aortic valve grows a viridans streptococcus from three sets because oral organisms adhered to an abnormal valve. A farm worker’s marrow grows a tiny oxidase-positive GNCB because Brucella lives inside macrophages. A pneumococcal bacteremia looks mucoid because capsule is the virulence factor you just identified with optochin.

Safety that is also pathogenicity

Virulence and laboratory safety collide at Brucella (and Francisella). A low infectious dose by aerosol is itself a virulence property. The correct bench behavior is containment: BSC, no sniffing, no open automated ID until rule-out is complete. That sentence is as much an II.A answer as “protein A binds Fc.”

Endocarditis, marrow pathogens, and virulence are one chapter of decision-making: name the organism with the tests you already know, map it onto valve versus marrow versus catheter, and never let a fastidious Gram-negative coccobacillus leave the cabinet as a casual MALDI spot.