Last updated
Other namesThrombocytopaenia, thrombopenia
Thrombocytopenia 1.jpg
A photomicrograph of the blood showing thrombocytopenia
Specialty Hematology
CausesBone marrow not making enough platelets, body destroying platelets, spleen holding too many platelets [1]
Diagnostic method Complete blood count [1]
TreatmentNone, immunosuppressants, platelet transfusion, surgical removal of the spleen [1]

Thrombocytopenia is a condition characterized by abnormally low levels of platelets, also known as thrombocytes, in the blood. [2] It is the most common coagulation disorder among intensive care patients and is seen in 20% of medical patients and a third of surgical patients. [3]


A normal human platelet count ranges from 150,000 to 450,000 platelets per microliter of blood. [4] Values outside this range do not necessarily indicate disease. One common definition of thrombocytopenia requiring emergency treatment is a platelet count below 50,000 per microliter. [5] Thrombocytopenia can be contrasted with the conditions associated with an abnormally high level of platelets in the blood: thrombocythemia (when the cause is unknown), and thrombocytosis (when the cause is known). [6] [7]

Signs and symptoms

Petechia on the lower leg from thrombocytopenia Petechia lower leg2.jpg
Petechia on the lower leg from thrombocytopenia
Right upper limb with purpura caused by thrombocytopenia in person with septic shock Trombocitopenia 01.JPG
Right upper limb with purpura caused by thrombocytopenia in person with septic shock

Thrombocytopenia usually has no symptoms and is picked up on a routine complete blood count. Some individuals with thrombocytopenia may experience external bleeding such as nosebleeds, or bleeding gums. Some women may have heavier or longer periods or breakthrough bleeding. Bruising, particularly purpura in the forearms and petechiae in the feet, legs, and mucous membranes, may be caused by spontaneous bleeding under the skin. [8] [9]

Eliciting a full medical history is vital to ensure the low platelet count is not secondary to another disorder. Ensuring that the other blood cell types, such as red blood cells and white blood cells are not also suppressed, is also important. [8] Painless, round, and pinpoint (1 to 3 mm in diameter) petechiae usually appear and fade, and sometimes group to form ecchymoses. Larger than petechiae, ecchymoses are purple, blue, or yellow-green areas of skin that vary in size and shape. They can occur anywhere on the body. [8]

A person with this disease may also complain of malaise, fatigue, and general weakness (with or without accompanying blood loss). Acquired thrombocytopenia may be associated with the use of certain drugs. Inspection typically reveals evidence of bleeding (petechiae or ecchymoses), along with slow, continuous bleeding from any injuries or wounds. Adults may have large, blood-filled bullae in the mouth. [10] If the person's platelet count is between 30,000 and 50,000/mm3, bruising with minor trauma may be expected; if it is between 15,000 and 30,000/mm3, spontaneous bruising will be seen (mostly on the arms and legs). [11]


Thrombocytopenia can be inherited or acquired. [12]

Decreased production

Abnormally low platelet production may be caused by: [13]

Increased destruction

TTP Thrombi in patient with thrombotic thrombocytopenic purpura .jpg

Abnormally high rates of platelet destruction may be due to immune or nonimmune conditions, including: [15]


These medications can induce thrombocytopenia through direct myelosuppression: [16]

Other causes


Laboratory tests for thrombocytopenia might include full blood count, liver enzymes, kidney function, vitamin B12 levels, folic acid levels, erythrocyte sedimentation rate, and peripheral blood smear. If the cause for the low platelet count remains unclear, a bone marrow biopsy is usually recommended to differentiate cases of decreased platelet production from cases of peripheral platelet destruction. [23]

Thrombocytopenia in hospitalized alcoholics may be caused by spleen enlargement, folate deficiency, and most frequently, the direct toxic effect of alcohol on production, survival time, and function of platelets. [24] Platelet count begins to rise after 2 to 5 days' abstinence from alcohol. The condition is generally benign, and clinically significant hemorrhage is rare.[ citation needed ]

In severe thrombocytopenia, a bone marrow study can determine the number, size, and maturity of the megakaryocytes. This information may identify ineffective platelet production as the cause of thrombocytopenia and rule out a malignant disease process at the same time. [25]


Treatment is guided by the severity and specific cause of the disease. Treatment focuses on eliminating the underlying problem, whether that means discontinuing drugs suspected to cause it or treating underlying sepsis. Diagnosis and treatment of serious thrombocytopenia is usually directed by a hematologist. Corticosteroids may be used to increase platelet production. Lithium carbonate or folate may also be used to stimulate platelet production in the bone marrow. [26]

Platelet transfusions

Platelet transfusions may be suggested for people who have a low platelet count due to thrombocytopenia. [27]

Thrombotic thrombocytopenic purpura

Treatment of thrombotic thrombocytopenic purpura (TTP) is a medical emergency, since the associated hemolytic anemia and platelet activation can lead to kidney failure and changes in the level of consciousness. Treatment of TTP was revolutionized in the 1980s with the application of plasmapheresis. According to the Furlan-Tsai hypothesis, [28] this treatment works by removing antibodies against the von Willebrand factor-cleaving protease ADAMTS-13. The plasmapheresis procedure also adds active ADAMTS-13 protease proteins to the patient, restoring a normal level of von Willebrand factor multimers. Patients with persistent antibodies against ADAMTS-13 do not always manifest TTP, and these antibodies alone are not sufficient to explain how plasmapheresis treats TTP. [29]

Immune thrombocytopenic purpura

Oral petechiae/purpura - Immune thrombocytopenic purpura Oral petechiae.JPG
Oral petechiae/purpura - Immune thrombocytopenic purpura

Many cases of immune thrombocytopenic purpura (ITP) also known as idiopathic thrombocytopenic purpura, can be left untreated, and spontaneous remission (especially in children) is not uncommon. However, counts under 50,000 are usually monitored with regular blood tests, and those with counts under 10,000 are usually treated, as the risk of serious spontaneous bleeding is high with such low platelet counts. Any patient experiencing severe bleeding symptoms is also usually treated. The threshold for treating ITP has decreased since the 1990s; hematologists recognize that patients rarely spontaneously bleed with platelet counts greater than 10,000, although exceptions to this observation have been documented. [30] [31]

Thrombopoetin analogues have been tested extensively for the treatment of ITP. These agents had previously shown promise, but had been found to stimulate antibodies against endogenous thrombopoietin or lead to thrombosis. Romiplostim (trade name Nplate, formerly AMG 531) was found to be safe and effective for the treatment of ITP in refractory patients, especially those who relapsed following splenectomy. [32]

Heparin-induced thrombocytopenia

Discontinuation of heparin is critical in a case of heparin-induced thrombocytopenia (HIT). Beyond that, however, clinicians generally treat to avoid thrombosis. [33] Treatment may include a direct thrombin inhibitor, such as lepirudin or argatroban. Other blood thinners sometimes used in this setting include bivalirudin and fondaparinux. Platelet transfusions are not routinely used to treat HIT because thrombosis, not bleeding, is the primary problem. [34] Warfarin is not recommended until platelets have normalized. [34]

Congenital amegakaryocytic thrombocytopenia

Bone marrow/stem cell transplants are the only known cures for this genetic disease. Frequent platelet transfusions are required to keep the patient from bleeding to death before the transplant can be performed, although this is not always the case. [35]

Human induced pluripotent stem cell-derived platelets

Human induced pluripotent stem cell-derived platelets is a technology currently being researched by the private sector, in association with the Biomedical Advanced Research and Development Authority and the U.S. Department of Health and Human Services, that would create platelets outside the human body. [36]

Neonatal thrombocytopenia

Thrombocytopenia affects a few newborns, and its prevalence in neonatal intensive care units is high. Normally, it is mild and resolves without consequences. Most cases affect preterm birth infants and result from placental insufficiency and/or fetal hypoxia. Other causes, such as alloimmunity, genetics, autoimmunity, and infection, are less frequent. [37]

Thrombocytopenia that starts after the first 72 hours since birth is often the result of underlying sepsis or necrotizing enterocolitis. [37] In the case of infection, PCR tests may be useful for rapid pathogen identification and detection of antibiotic resistance genes. Possible pathogens include viruses (e.g. cytomegalovirus, [37] rubella virus, [37] HIV [37] ), bacteria (e.g. Staphylococcus spp., [38] Enterococcus spp., [38] Streptococcus agalactiae , [37] Listeria monocytogenes , [37] Escherichia coli , [37] [38] Haemophilus influenzae , [37] Klebsiella pneumoniae , [38] Pseudomonas aeruginosa , [38] [39] Yersinia enterocolitica [39] ), fungi (e.g. Candida spp. [38] ), and Toxoplasma gondii . [37] The severity of thrombocytopenia may be correlated with pathogen type; some research indicates that the most severe cases are related to fungal or Gram-negative bacterial infection. [38] The pathogen may be transmitted during [40] or before birth, by breast feeding, [41] [42] [43] or during transfusion. [44] Interleukin-11 is being investigated as a drug for managing thrombocytopenia, especially in cases of sepsis or necrotizing enterocolitis. [37]

Related Research Articles

Disseminated intravascular coagulation Medical condition

Disseminated intravascular coagulation (DIC) is a condition in which blood clots form throughout the body, blocking small blood vessels. Symptoms may include chest pain, shortness of breath, leg pain, problems speaking, or problems moving parts of the body. As clotting factors and platelets are used up, bleeding may occur. This may include blood in the urine, blood in the stool, or bleeding into the skin. Complications may include organ failure.

Immune thrombocytopenic purpura Medical condition

Immune thrombocytopenic purpura (ITP), also known as idiopathic thrombocytopenic purpura or immune thrombocytopenia, is a type of thrombocytopenic purpura defined as an isolated low platelet count with a normal bone marrow in the absence of other causes of low platelets. It causes a characteristic red or purple bruise-like rash and an increased tendency to bleed. Two distinct clinical syndromes manifest as an acute condition in children and a chronic condition in adults. The acute form often follows an infection and spontaneously resolves within two months. Chronic immune thrombocytopenia persists longer than six months with a specific cause being unknown.

Thrombotic thrombocytopenic purpura Medical condition

Thrombotic thrombocytopenic purpura (TTP) is a blood disorder that results in blood clots forming in small blood vessels throughout the body. This results in a low platelet count, low red blood cells due to their breakdown, and often kidney, heart, and brain dysfunction. Symptoms may include large bruises, fever, weakness, shortness of breath, confusion, and headache. Repeated episodes may occur.

Hemolytic–uremic syndrome Group of blood disorders related to bacterial infection

Hemolytic–uremic syndrome (HUS) is a group of blood disorders characterized by low red blood cells, acute kidney failure, and low platelets. Initial symptoms typically include bloody diarrhea, fever, vomiting, and weakness. Kidney problems and low platelets then occur as the diarrhea progresses. Children are more commonly affected, but most children recover without permanent damage to their health, although some children may have serious and sometimes life-threatening complications. Adults, especially the elderly, may present a more complicated presentation. Complications may include neurological problems and heart failure.

von Willebrand factor Mammalian protein involved in blood clotting

von Willebrand factor (VWF) is a blood glycoprotein involved in hemostasis, specifically, platelet adhesion. It is deficient and/or defective in von Willebrand disease and is involved in many other diseases, including thrombotic thrombocytopenic purpura, Heyde's syndrome, and possibly hemolytic–uremic syndrome. Increased plasma levels in many cardiovascular, neoplastic, metabolic, and connective tissue diseases are presumed to arise from adverse changes to the endothelium, and may predict an increased risk of thrombosis.

Wiskott–Aldrich syndrome Medical condition

Wiskott–Aldrich syndrome (WAS) is a rare X-linked recessive disease characterized by eczema, thrombocytopenia, immune deficiency, and bloody diarrhea. It is also sometimes called the eczema-thrombocytopenia-immunodeficiency syndrome in keeping with Aldrich's original description in 1954. The WAS-related disorders of X-linked thrombocytopenia (XLT) and X-linked congenital neutropenia (XLN) may present with similar but less severe symptoms and are caused by mutations of the same gene.

Plateletpheresis Method of collecting platelets from blood

Plateletpheresis is the process of collecting thrombocytes, more commonly called platelets, a component of blood involved in blood clotting. The term specifically refers to the method of collecting the platelets, which is performed by a device used in blood donation that separates the platelets and returns other portions of the blood to the donor. Platelet transfusion can be a life-saving procedure in preventing or treating serious complications from bleeding and hemorrhage in patients who have disorders manifesting as thrombocytopenia or platelet dysfunction. This process may also be used therapeutically to treat disorders resulting in extraordinarily high platelet counts such as essential thrombocytosis.

Evans syndrome is an autoimmune disease in which an individual's immune system attacks their own red blood cells and platelets, the syndrome can include immune neutropenia. These immune cytopenias may occur simultaneously or sequentially.

Schistocyte Fragmented portion of a red blood cell

A schistocyte or schizocyte is a fragmented part of a red blood cell. Schistocytes are typically irregularly shaped, jagged, and have two pointed ends.

ADAMTS13 Metalloprotease enzyme

ADAMTS13 —also known as von Willebrand factor-cleaving protease (VWFCP)—is a zinc-containing metalloprotease enzyme that cleaves von Willebrand factor (vWf), a large protein involved in blood clotting. It is secreted into the blood and degrades large vWf multimers, decreasing their activity.

Mean platelet volume (MPV) is a machine-calculated measurement of the average size of platelets found in blood and is typically included in blood tests as part of the CBC. Since the average platelet size is larger when the body is producing increased numbers of platelets, the MPV test results can be used to make inferences about platelet production in bone marrow or platelet destruction problems.

Thrombotic microangiopathy Medical condition

Thrombotic microangiopathy (TMA) is a pathology that results in thrombosis in capillaries and arterioles, due to an endothelial injury. It may be seen in association with thrombocytopenia, anemia, purpura and kidney failure.

Neonatal alloimmune thrombocytopenia is a disease that affects babies in which the platelet count is decreased because the mother's immune system attacks her fetus' or newborn's platelets. A low platelet count increases the risk of bleeding in the fetus and newborn. If the bleeding occurs in the brain, there may be long-term effects.

John W. Semple is a Canadian Scientist at St. Michael's Hospital and a Professor of Pharmacology at the University of Toronto. He was born in Windsor, Ontario in 1959 and received his PhD in Immunology at Queen's University at Kingston, Ontario. In 1991, Semple, along with John Freedman, discovered a T helper cell defect in patients with the bleeding disorder called immune thrombocytopenic purpura (ITP). ITP is the condition of having a low platelet count (thrombocytopenia) and most causes appear to be related to antibodies against platelets. Very low platelet counts can lead to a bleeding diathesis and purpura. The T cell defect was initially shown to be an exaggerated interleukin-2 response when T cells were cultured with platelets in vitro. Subsequently, this cytokine abnormality was shown by others to be responsible for many of the autoimmune mechanisms causing the disorder.). The importance of understanding the T cell defects in ITP is that novel therapies aimed at these cells may significantly benefit patients with ITP.

Eltrombopag Chemical compound

Eltrombopag, sold under the brand name Promacta among others, is a medication used to treat thrombocytopenia and severe aplastic anemia. Promacta (eltrombopag) is known as Revolade® outside the U.S. and is marketed worldwide by Novartis.

The Harrington–Hollingsworth experiment was an experiment that established the autoimmune nature of the blood disorder immune thrombocytopenic purpura. It was performed in 1950 by the academic staff of Barnes-Jewish Hospital in St. Louis, Missouri.

Hematologic diseases are disorders which primarily affect the blood & blood-forming organs. Hematologic diseases include rare genetic disorders, anemia, HIV, sickle cell disease & complications from chemotherapy or transfusions.

Fostamatinib Chemical compound

Fostamatinib, sold under the brand names Tavalisse and Tavlesse, is a tyrosine kinase inhibitor medication for the treatment of chronic immune thrombocytopenia (ITP). The drug is administered by mouth.

Giant platelet disorder Medical condition

Giant platelet disorders, also known as macrothrombocytopenia, are rare disorders featuring abnormally large platelets, thrombocytopenia and a tendency to bleeding. Giant platelets cannot stick adequately to an injured blood vessel walls, resulting in abnormal bleeding when injured. Giant platelet disorder occurs for inherited diseases like Bernard–Soulier syndrome, gray platelet syndrome and May–Hegglin anomaly.

Upshaw–Schulman syndrome Medical condition

Upshaw–Schulman syndrome (USS) is the recessively inherited form of thrombotic thrombocytopenic purpura (TTP), a rare and complex blood coagulation disease. USS is caused by the absence of the ADAMTS13 protease resulting in the persistence of ultra large von Willebrand factor multimers (ULVWF), causing episodes of acute thrombotic microangiopathy with disseminated multiple small vessel obstructions. These obstructions deprive downstream tissues from blood and oxygen, which can result in tissue damage and death. The presentation of an acute USS episode is variable but usually associated with thrombocytopenia, microangiopathic hemolytic anemia (MAHA) with schistocytes on the peripheral blood smear, fever and signs of ischemic organ damage in the brain, kidney and heart.


  1. 1 2 3 "Thrombocytopenia". National Heart, Lung, and Blood Institute. Retrieved 4 January 2018.
  2. Deutschman, Clifford S.; Neligan, Patrick J. (2010). Evidence-based Practice of Critical Care. Elsevier Health Sciences. ISBN   978-1416054764 . Retrieved 2015-04-30.
  3. Marini, John J; Dries, David J (2019). Critical care medicine: the essentials and more. Philadelphia: Wolters Kluwer. ISBN   978-1-4963-0291-5. OCLC   1060947164.
  4. "Platelet count: MedlinePlus Medical Encyclopedia". Retrieved 2015-05-01.
  5. "What Is Thrombocytopenia? - NHLBI, NIH". Retrieved 2015-05-01.
  6. Schafer AI (March 2004). "Thrombocytosis". N. Engl. J. Med. 350 (12): 1211–9. doi:10.1056/NEJMra035363. PMID   15028825.
  7. "Thrombocythemia and Thrombocytosis | NHLBI, NIH". Retrieved 5 August 2020.
  8. 1 2 3 Bhatia, M.P.S. "B.E. Project on Platlet Count Using Image Processing Techniques" (PDF). BTP_Report. Retrieved 30 November 2014.
  9. Houghton, Andrew R.; Gray, David (2010). Chamberlain's Symptoms and Signs in Clinical Medicine 13th Edition, An Introduction to Medical Diagnosis. CRC Press. ISBN   9780340974254 . Retrieved 2015-05-01.
  10. Interpreting Signs and Symptoms. Lippincott Williams & Wilkins. 2007. p. 293. ISBN   9781582556680.
  11. Rosdahl, Caroline Bunker; Kowalski, Mary T. (2008). Textbook of Basic Nursing. Lippincott Williams & Wilkins. ISBN   9780781765213 . Retrieved 2015-05-01.
  12. "What Causes Thrombocytopenia?". National Heart, Lung, and Blood Institute. Retrieved 4 December 2014.
  13. Fiebach, Nicholas H.; Barker, Lee Randol; Burton, John Russell; Zieve, Philip D. (2007). Principles of Ambulatory Medicine. Lippincott Williams & Wilkins. ISBN   9780781762274 . Retrieved 2015-04-30.
  14. Almazni I, Stapley R, Morgan NV (2019) Inherited Thrombocytopenia: Update on genes and genetic variants which may be associated With bleeding. Front Cardiovasc Med
  15. Rodak, Bernadette F.; Fritsma, George A.; Keohane, Elaine (2013). Hematology: Clinical Principles and Applications. Elsevier Health Sciences. ISBN   9780323292696 . Retrieved 2015-04-30.
  16. Gresele, Paolo; Fuster, Valentin; Lopez, Jose A.; Page, Clive P.; Vermylen, Jos (2007). Platelets in Hematologic and Cardiovascular Disorders: A Clinical Handbook. Cambridge University Press. ISBN   9781139468763 . Retrieved 2015-04-30.
  17. Tan, GC; Stalling, M; Dennis, G; Nunez, M; Kahwash, SB (2016). "Pseudothrombocytopenia due to Platelet Clumping: A Case Report and Brief Review of the Literature". Case Reports in Hematology. 2016: 1–4. doi: 10.1155/2016/3036476 . PMC   5164902 . PMID   28044112.
  18. Waldmann, Carl; Soni, Neil; Rhodes, Andrew (2008). Oxford Desk Reference: Critical Care. Oxford University Press. ISBN   9780199229581 . Retrieved 2015-05-01.
  19. Dart, Richard C. (2004). Medical Toxicology. Lippincott Williams & Wilkins. ISBN   9780781728454 . Retrieved 2015-05-01.
  20. Greer, John P.; Arber, Daniel A.; Glader, Bertil; List, Alan F.; Means, Robert T.; Paraskevas, Frixos; Rodgers, George M. (2013). Wintrobe's Clinical Hematology. Lippincott Williams & Wilkins. ISBN   9781469846224 . Retrieved 2015-05-01.
  21. "Niemann-Pick disease". Genetics Home Reference.
  22. "Niemann-Pick - Symptoms and causes". Mayo Clinic .
  23. "How Is Thrombocytopenia Diagnosed? - NHLBI, NIH". Retrieved 2015-05-19.
  24. Lieber, Charles S. (2012). Medical and Nutritional Complications of Alcoholism: Mechanisms and Management. Springer Science & Business Media. ISBN   9781461533207.
  25. Hillyer, Christopher D.; Abrams, Charles S.; Shaz, Beth H.; Roshal, Mikhail; Zimring, James C.; Abshire, Thomas C. (2009). Transfusion Medicine and Hemostasis: Clinical and Laboratory Aspects. Elsevier. ISBN   9780080922300 . Retrieved 2015-05-01.
  26. Lawrence, Peter F.; Bell, Richard M.; Dayton, Merril T. (2012-10-31). Essentials of General Surgery. Lippincott Williams & Wilkins. ISBN   9780781784955.
  27. Estcourt, Lise J; Malouf, Reem; Hopewell, Sally; Doree, Carolyn; Van Veen, Joost (2018-04-30). Cochrane Haematological Malignancies Group (ed.). "Use of platelet transfusions prior to lumbar punctures or epidural anaesthesia for the prevention of complications in people with thrombocytopenia". Cochrane Database of Systematic Reviews. 4: CD011980. doi:10.1002/14651858.CD011980.pub3. PMC   5957267 . PMID   29709077.
  28. Chapman, Kent; Seldon, Michael; Richards, Ross (2012). "Thrombotic microangiopathies, thrombotic thrombocytopenic purpura, and ADAMTS-13". Seminars in Thrombosis and Hemostasis. 38 (1): 47–54. doi: 10.1055/s-0031-1300951 . PMID   22314603.
  29. "How Is Thrombotic Thrombocytopenic Purpura Treated? - NHLBI, NIH". Retrieved 2015-05-20.
  30. Thrombocytopenic Purpura: New Insights for the Healthcare Professional: 2013 Edition: ScholarlyPaper. ScholarlyEditions. 2013-07-22. ISBN   9781481662420.
  31. "Idiopathic thrombocytopenic purpura (ITP): MedlinePlus Medical Encyclopedia". Retrieved 2015-05-20.
  32. "Nplate (romiplostim) for subcutaneous injection". Retrieved 2015-05-02.
  33. Warkentin, Theodore E.; Greinacher, Andreas (2007-07-23). Heparin-Induced Thrombocytopenia. CRC Press. ISBN   9781439826423.
  34. 1 2 Ahmed, I; Majeed, A; Powell, R (2007). "Heparin induced thrombocytopenia: diagnosis and management update". Postgraduate Medical Journal. 83 (983): 575–582. doi:10.1136/pgmj.2007.059188. ISSN   0032-5473. PMC   2600013 . PMID   17823223.
  35. Smit-Sibinga, C. Th (2010-05-10). Neonatology and Blood Transfusion. Springer Science & Business Media. ISBN   9780387236001.
  36. Clark, Douglas (2019-10-02). "New technology may aid emergency preparedness". Homeland Preparedness News. Retrieved 2019-10-23.
  37. 1 2 3 4 5 6 7 8 9 10 11 Roberts, I; Murray, N. A. (2003). "Neonatal thrombocytopenia: causes and management". Archives of Disease in Childhood: Fetal and Neonatal Edition. 88 (5): F359–64. doi:10.1136/fn.88.5.F359. ISSN   1468-2052. PMC   1721612 . PMID   12937037.
  38. 1 2 3 4 5 6 7 Guida, JD; Kunig, AM; Leef, KH; McKenzie, SE; Paul, DA (2003). "Platelet count and sepsis in very low birth-weight neonates: is there an organism-specific response?". Pediatrics. 111 (6 Pt 1): 1411–15. doi:10.1542/peds.111.6.1411. PMID   12777561.
  39. 1 2 Pacifico, L; Chiesa, C; Mirabella, S; Panero, A; Midulla, M (1987). "Early-onset Pseudomonas aeruginosa sepsis and Yersinia enterocolitica neonatal infection: a unique combination in a preterm infant". European Journal of Pediatrics. 146 (2): 192–93. doi:10.1007/BF02343233. PMID   3569360. S2CID   20198866.
  40. Rempen, A; Martius, J; Hartmann, AA; Wecker, I (1987). "Transmission rate of Ureaplasma urealyticum, Mycoplasma spp., Gardnerella vaginalis, B-streptococci, Candida spp. and Chlamydia trachomatis from the mother to the newborn". Archives of Gynecology and Obstetrics. 241 (3): 165–70. doi:10.1007/BF00931313. PMID   3324978. S2CID   11251976.
  41. Olver, WJ; Bond, DW; Boswell, TC; Watkin, SL (2000). "Neonatal group B streptococcal disease associated with infected breast milk". Archives of Disease in Childhood: Fetal and Neonatal Edition. 83 (1): F48–49. doi:10.1136/fn.83.1.F48. PMC   1721104 . PMID   10873172.
  42. Kotiw, M; Zhang, GW; Daggard, G; Reiss-Levy, E; Tapsall, JW; Numa, A (2003). "Late-onset and recurrent neonatal Group B streptococcal disease associated with breast-milk transmission". Pediatric and Developmental Pathology. 6 (3): 251–56. doi:10.1007/s10024-001-0276-y. PMID   12687430. S2CID   20696142.
  43. Gastelum, DT; Dassey, D; Mascola, L; Yasuda, LM (2005). "Transmission of community-associated methicillin-resistant Staphylococcus aureus from breast milk in the neonatal intensive care unit". The Pediatric Infectious Disease Journal. 24 (12): 1122–24. doi:10.1097/01.inf.0000189983.71585.30. PMID   16371885.
  44. Jagielski, Marek; Rastawicki, Waldemar; Kałużewski, Stanisław; Gierczyński, Rafał (2007). "Jersinioza – niedoceniana choroba zakaźna" [Yersiniosis – unappreciated infectious diseases](PDF). Przegl Epidemiol (in Polish). 56 (1): 57–64. PMID   12150068. Archived from the original (PDF) on 2011-10-03. Retrieved 2011-04-10.