Bartonella, Borrelia or Lyme, Babesia, and the Heart

How Three Tick-Borne Germs Live In and Damage the Heart’s Tiny Blood Vessels

Your heart is fed by a network of extremely small blood vessels called capillaries. They are so narrow that red blood cells have to squeeze through them one at a time. Three germs spread by ticks — Borrelia (Lyme disease), Bartonella, and Babesia — can all cause trouble in this network, but each one does it in a completely different way.

Here is the short version before the details:

GermWhere it livesWhat it does to the heart
Borrelia (Lyme)Outside of cells, stuck to vessel walls and nearby tissueCauses inflammation that blocks the heart’s electrical signals
BartonellaInside red blood cells and inside vessel-wall cellsGrows extra vessel tissue, infects heart valves
BabesiaOnly inside red blood cellsMakes blood cells stiff, clogging capillaries

1. Borrelia burgdorferi — The Lyme Disease Germ

How It Gets Into the Heart

1.1 It grabs onto vessel walls. Borrelia is a long, spiral-shaped bacterium that swims through the bloodstream. It uses sticky surface proteins (one is called BBK32) to grab the inner lining of blood vessels. Scientists watched this happen live in mice: the germ briefly touches the wall, lets go, touches again, and finally holds on tight. It’s a lot like the way white blood cells roll along a vessel wall before stopping.¹⁻³

1.2 It slips through the wall. Once attached, it squeezes between the cells of the vessel lining, or sometimes passes straight through a cell. It doesn’t live inside those cells — it just passes through on its way out of the bloodstream.⁴⁻⁶

1.3 It carries its own “scissors.” The germ grabs a human protein called plasminogen and turns it into plasmin, a natural enzyme that cuts through tissue. This helps the germ tunnel through the tough layers surrounding blood vessels.⁷

1.4 It hides in tough tissue. Borrelia sticks to collagen-rich material in the tissue around vessels and in heart valves. This is a good hiding spot because antibodies and antibiotics don’t reach it well there.⁸⁻¹⁰

What That Does to the Heart

1.5 The vessel lining gets “angry.” Infected lining cells put out sticky flags and chemical signals that call immune cells in. Those immune cells crowd into the heart tissue, and that crowding is the actual damage.¹¹

1.6 It goes for the heart’s wiring. The germ gathers near the base of the wall between the two lower heart chambers — exactly where the heart’s electrical relay station (the AV node) sits. The result is heart block: electrical signals get delayed or blocked, and the heart beats too slowly. A key feature is that it can change hour to hour and usually goes away completely with treatment.¹²⁻¹⁴

1.7 Inflammation through the whole heart wall. Autopsy studies show immune cells spread from the inner lining all the way out to the outer covering, with the actual spirochetes visible under special stains.¹²,¹⁵

1.8 It can kill suddenly. Rare but real: young, healthy people have died of Lyme carditis, sometimes with almost no warning symptoms beforehand.¹⁵,¹⁶

1.9 Long-term weakening of the heart muscle. Some people, mostly in Europe, develop an enlarged, weak heart. Lyme DNA has been found in heart muscle samples from a few of these patients. Whether Lyme truly caused it is still argued about.¹⁷,¹⁸

1.10 Other heart areas. The sac around the heart can become inflamed and fill with fluid, and valves can occasionally be affected.¹⁹

2. Bartonella — The Vessel-Wall Specialist

This is the only one of the three that truly moves in and lives inside blood vessel wall cells.

Its Two Hiding Places

2.1 Inside red blood cells. Bartonella uses special tools (the IalB protein and a syringe-like system called Trw) to force its way into red blood cells. Once inside, it mostly stops multiplying and just sits there. Your immune system can’t see it, and antibiotics have a hard time reaching it. Every so often it comes back out, which is why the infection in the blood comes in waves.²⁰⁻²²

2.2 Inside vessel-wall cells — the “invasome.” Here’s something strange: instead of entering one at a time, the bacteria clump into a big ball on the surface of a vessel-lining cell. The cell then rearranges its own internal skeleton and swallows the whole clump. Scientists named this structure the invasome.²³,²⁴

2.3 It stops its host cell from dying. Infected cells normally self-destruct to protect the body. Bartonella injects proteins that switch off that self-destruct program, so the infected cell lives longer and the germ keeps its home.²⁵

2.4 It makes the body grow extra blood vessels. This is its signature trick. It flips on growth signals (VEGF and others) that make vessel-lining cells multiply. You get lumpy, overgrown blood vessel tissue, and the overgrowth physically narrows and squeezes the capillary openings.²⁶,²⁷

2.5 Blood-filled pockets in organs. The same overgrowth process inside the liver and spleen creates blood-filled cavities.²⁶

What That Does to the Heart

2.6 Valve infection that standard blood tests miss. Bartonella is one of the top causes of infective endocarditis where normal blood cultures come back negative. It strongly favors the aortic valve, builds large destructive clumps on it, and often damages the valve badly enough that surgery is needed. Diagnosis usually requires antibody tests or DNA testing of the removed valve.²⁸⁻³⁰

2.7 Heart muscle inflammation can happen even without obvious clumps on a valve.³⁰

2.8 Kidney damage and false alarms. Immune complexes build up and inflame the kidneys. The blood test pattern looks so much like an autoimmune disease that patients are sometimes misdiagnosed with vasculitis and given immune-suppressing drugs — which is exactly the wrong treatment for an infection.³¹

2.9 Pieces break off. Fragments of the valve clumps can travel in the bloodstream and block vessels elsewhere, including in the brain.²⁹

3. Babesia — The Red Blood Cell Parasite

How It Clogs the Microcirculation

3.1 It can only live inside red blood cells. Babesia is a parasite, not a bacterium. It invades a red blood cell, multiplies inside, bursts the cell open, and the new parasites invade fresh cells. The cycle repeats.³²

3.2 It makes red blood cells stiff. Healthy red blood cells are flexible and bend to fit through capillaries. Infected ones become rigid. Stiff cells get stuck, traffic backs up, and blood flow through the capillary beds slows down. This is the main problem Babesia causes.³³,³⁴

3.3 Infected cells can stick to vessel walls. Best proven in the cattle version of the parasite, which puts a sticky protein on the red cell surface and changes it constantly to dodge the immune system. Infected cells pile up in brain and lung capillaries. In humans this is less well studied, but congestion is clearly seen.³⁵,³⁶

3.4 Free hemoglobin causes damage. When red cells burst, hemoglobin spills into the plasma. Loose hemoglobin mops up nitric oxide — the molecule blood vessels use to relax and open up. Without it, vessels stay tight and the lining gets injured.³⁷

3.5 The immune response adds to it. Inflammatory signals (TNF-α, IFN-γ, IL-6) make capillaries leaky, which drives many of the serious complications.³⁸

3.6 Fluid in the lungs. Severe cases can develop lung failure from leaking capillaries. Oddly, this often appears after treatment starts, as dying parasites trigger a burst of inflammation.³⁹,⁴⁰

3.7 Widespread clotting. The clotting system can go haywire, forming tiny clots throughout the body’s small vessels.³⁹

3.8 Heart strain. Babesia doesn’t infect heart muscle. Instead, severe anemia plus clogged capillaries means the heart gets far less oxygen than it needs while working harder. Heart attacks, raised troponin levels, and heart failure have all been reported. The spleen can also be damaged or rupture.⁴¹,⁴²

3.9 Who gets the worst disease. People without a spleen, those over 50, those on immune-suppressing drugs (especially rituximab), and cancer patients.⁴⁰,⁴³

4. The Big Picture

Three different ways to wreck a capillary:

  • Bartonella — narrows it by growing extra tissue into the opening
  • Babesia — clogs it with stiff, sticky red blood cells
  • Borrelia — crowds it with inflammation in the surrounding tissue

Only Bartonella actually lives and multiplies inside vessel-wall cells. Borrelia just passes through them, and Babesia never touches them.

Co-infection is common because the same tick can carry more than one germ, and symptoms can overlap and get confusing. But there is currently no solid human evidence that they team up to make heart vessel damage worse.⁴⁴,⁴⁵

Each one needs a different test. Bartonella valve infection needs antibody tests plus DNA testing of the valve. Lyme carditis needs the two-step antibody test plus an ECG in anyone suspected of having it. Babesiosis needs a blood smear plus DNA testing, with a count of how many cells are infected.⁴⁶⁻⁴⁸

Endnotes

  1. Moriarty TJ, Norman MU, Colarusso P, Bankhead T, Kubes P, Chaconas G. Real-time high resolution 3D imaging of the Lyme disease spirochete adhering to and escaping from the vasculature of a living host. PLoS Pathogens. 2008;4(6):e1000090.
  2. Norman MU, Moriarty TJ, Dresser AR, Millen B, Kubes P, Chaconas G. Molecular mechanisms involved in vascular interactions of the Lyme disease pathogen in a living host. PLoS Pathogens. 2008;4(10):e1000169.
  3. Probert WS, Johnson BJB. Identification of a 47 kDa fibronectin-binding protein expressed by Borrelia burgdorferi isolate B31. Molecular Microbiology. 1998;30(5):1003–1015.
  4. Comstock LE, Thomas DD. Penetration of endothelial cell monolayers by Borrelia burgdorferi. Infection and Immunity. 1989;57(5):1626–1628.
  5. Ma Y, Sturrock A, Weis JJ. Intracellular localization of Borrelia burgdorferi within human endothelial cells. Infection and Immunity. 1991;59(2):671–678.
  6. Szczepanski A, Furie MB, Benach JL, Lane BP, Fleit HB. Interaction between Borrelia burgdorferi and endothelium in vitro. Journal of Clinical Investigation. 1990;85(5):1637–1647.
  7. Coleman JL, Gebbia JA, Piesman J, Degen JL, Bugge TH, Benach JL. Plasminogen is required for efficient dissemination of B. burgdorferi in ticks and for enhancement of spirochetemia in mice. Cell. 1997;89(7):1111–1119.
  8. Guo BP, Brown EL, Dorward DW, Rosenberg LC, Höök M. Decorin-binding adhesins from Borrelia burgdorferi. Molecular Microbiology. 1998;30(4):711–723.
  9. Shi Y, Xu Q, McShan K, Liang FT. Both decorin-binding proteins A and B are critical for overall virulence of Borrelia burgdorferi. Infection and Immunity. 2008;76(3):1239–1246.
  10. Parveen N, Leong JM. Identification of a candidate glycosaminoglycan-binding adhesin of the Lyme disease spirochete. Molecular Microbiology. 2000;35(5):1220–1234.
  11. Sellati TJ, Abrescia LD, Radolf JD, Furie MB. Outer surface lipoproteins of Borrelia burgdorferi activate vascular endothelium in vitro. Infection and Immunity. 1996;64(9):3180–3187.
  12. Reznick JW, Braunstein DB, Walsh RL, et al. Lyme carditis: electrophysiologic and histopathologic study. American Journal of Medicine. 1986;81(5):923–927.
  13. Steere AC, Batsford WP, Weinberg M, et al. Lyme carditis: cardiac abnormalities of Lyme disease. Annals of Internal Medicine. 1980;93(1):8–16.
  14. Yeung C, Baranchuk A. Diagnosis and treatment of Lyme carditis: JACC review topic of the week. Journal of the American College of Cardiology. 2019;73(6):717–726.
  15. Muehlenbachs A, Bollweg BC, Schulz TJ, et al. Cardiac tropism of Borrelia burgdorferi: an autopsy study of sudden cardiac death associated with Lyme carditis. American Journal of Pathology. 2016;186(5):1195–1205.
  16. Centers for Disease Control and Prevention. Three sudden cardiac deaths associated with Lyme carditis — United States, November 2012–July 2013. MMWR. 2013;62(49):993–996.
  17. Stanek G, Klein J, Bittner R, Glogar D. Isolation of Borrelia burgdorferi from the myocardium of a patient with longstanding cardiomyopathy. New England Journal of Medicine. 1990;322(4):249–252.
  18. Klein J, Stanek G, Bittner R, Horvat R, Holzinger C, Glogar D. Lyme borreliosis as a cause of myocarditis and myocardial dilatation. European Heart Journal. 1991;12(Suppl D):73–75.
  19. Kostić T, Momčilović S, Perišić ZD, et al. Manifestations of Lyme carditis. International Journal of Cardiology. 2017;232:24–32.
  20. Coleman SA, Minnick MF. Establishing a direct role for the Bartonella bacilliformis invasion-associated locus B (IalB) protein in human erythrocyte parasitism. Infection and Immunity. 2001;69(7):4373–4381.
  21. Vayssier-Taussat M, Le Rhun D, Deng HK, et al. The Trw type IV secretion system of Bartonella mediates host-specific adhesion to erythrocytes. PLoS Pathogens. 2010;6(6):e1000946.
  22. Schülein R, Seubert A, Gille C, et al. Invasion and persistent intracellular colonization of erythrocytes: a unique parasitic strategy of the emerging pathogen Bartonella. Journal of Experimental Medicine. 2001;193(9):1077–1086.
  23. Dehio C, Meyer M, Berger J, Schwarz H, Lanz C. Interaction of Bartonella henselae with endothelial cells results in bacterial aggregation on the cell surface and the subsequent engulfment and internalisation of the bacterial aggregate by a unique structure, the invasome. Journal of Cell Science. 1997;110(18):2141–2154.
  24. Riess T, Andersson SGE, Lupas A, et al. Bartonella adhesin A mediates a proangiogenic host cell response. Journal of Experimental Medicine. 2004;200(10):1267–1278.
  25. Schmid MC, Scheidegger F, Dehio M, et al. A translocated bacterial protein protects vascular endothelial cells from apoptosis. PLoS Pathogens. 2006;2(11):e115.
  26. Dehio C. Bartonella interactions with endothelial cells and erythrocytes. Trends in Microbiology. 2001;9(6):279–285.
  27. Kempf VAJ, Lebiedziejewski M, Alitalo K, et al. Activation of hypoxia-inducible factor-1 in bacillary angiomatosis: evidence for a role of hypoxia-inducible factor-1 in bacterial infections. Circulation. 2005;111(8):1054–1062.
  28. Raoult D, Fournier PE, Vandenesch F, et al. Outcome and treatment of Bartonella endocarditis. Archives of Internal Medicine. 2003;163(2):226–230.
  29. Fournier PE, Lelievre H, Eykyn SJ, et al. Epidemiologic and clinical characteristics of Bartonella quintana and Bartonella henselae endocarditis: a study of 48 patients. Medicine (Baltimore). 2001;80(4):245–251.
  30. Okaro U, Addisu A, Casanas B, Anderson B. Bartonella species, an emerging cause of blood-culture-negative endocarditis. Clinical Microbiology Reviews. 2017;30(3):709–746.
  31. Boils CL, Nasr SH, Walker PD, Couser WG, Larsen CP. Update on endocarditis-associated glomerulonephritis. Kidney International. 2015;87(6):1241–1249.
  32. Vannier E, Krause PJ. Human babesiosis. New England Journal of Medicine. 2012;366(25):2397–2407.
  33. Clark IA, Jacobson LS. Do babesiosis and malaria share a common disease process? Annals of Tropical Medicine and Parasitology. 1998;92(4):483–488.
  34. Jacobson LS, Clark IA. The pathophysiology of canine babesiosis: new approaches to an old puzzle. Journal of the South African Veterinary Association. 1994;65(3):134–145.
  35. Allred DR, Carlton JMR, Satcher RL, et al. The ves multigene family of B. bovis encodes components of rapid antigenic variation at the infected erythrocyte surface. Molecular Cell. 2000;5(1):153–162.
  36. O’Connor RM, Long JA, Allred DR. Cytoadherence of Babesia bovis-infected erythrocytes to bovine brain capillary endothelial cells provides an in vitro model for sequestration. Infection and Immunity. 1999;67(8):3921–3928.
  37. Rother RP, Bell L, Hillmen P, Gladwin MT. The clinical sequelae of intravascular hemolysis and extracellular plasma hemoglobin: a novel mechanism of human disease. JAMA. 2005;293(13):1653–1662.
  38. Krause PJ, Daily J, Telford SR, Vannier E, Lantos P, Spielman A. Shared features in the pathobiology of babesiosis and malaria. Trends in Parasitology. 2007;23(12):605–610.
  39. Hatcher JC, Greenberg PD, Antique J, Jimenez-Lucho VE. Severe babesiosis in Long Island: review of 34 cases and their complications. Clinical Infectious Diseases. 2001;32(8):1117–1125.
  40. White DJ, Talarico J, Chang HG, Birkhead GS, Heimberger T, Morse DL. Human babesiosis in New York State: review of 139 hospitalized cases and analysis of prognostic factors. Archives of Internal Medicine. 1998;158(19):2149–2154.
  41. Reis F, Pestana Santos C, Correia H. Babesiosis and myocardial infarction: a rare association. BMJ Case Reports. 2019;12(7):e229588.
  42. Florescu D, Sordillo PP, Glyptis A, et al. Splenic infarction in human babesiosis: two cases and discussion. Clinical Infectious Diseases. 2008;46(1):e8–e11.
  43. Vannier EG, Diuk-Wasser MA, Ben Mamoun C, Krause PJ. Babesiosis. Infectious Disease Clinics of North America. 2015;29(2):357–370.
  44. Krause PJ, Telford SR, Spielman A, et al. Concurrent Lyme disease and babesiosis: evidence for increased severity and duration of illness. JAMA. 1996;275(21):1657–1662.
  45. Diuk-Wasser MA, Vannier E, Krause PJ. Coinfection by Ixodes tick-borne pathogens: ecological, epidemiological, and clinical consequences. Trends in Parasitology. 2016;32(1):30–42.
  46. Lantos PM, Rumbaugh J, Bockenstedt LK, et al. Clinical practice guidelines by IDSA, AAN, and ACR: 2020 guidelines for the prevention, diagnosis and treatment of Lyme disease. Clinical Infectious Diseases. 2021;72(1):e1–e48.
  47. Krause PJ, Auwaerter PG, Bannuru RR, et al. Clinical practice guidelines by IDSA: 2020 guideline on diagnosis and management of babesiosis. Clinical Infectious Diseases. 2021;72(2):e49–e64.
  48. Baddour LM, Wilson WR, Bayer AS, et al. Infective endocarditis in adults: diagnosis, antimicrobial therapy, and management of complications. Circulation. 2015;132(15):1435–1486.

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