Petechiae & Purpura
Petechiae
A pinpoint, nonraised, perfectly round, purplish red spot caused by intradermal or submucous haemorrhage. Petechiae information and photos here and here.
Tick Borne Disease Relationship- Petechiae
Parvovirus B19 has been described recently to cause generalized petechiae. The differential diagnosis includes allergic contact dermatitis, rickettsial infections and Kawasaki disease. Treatment is symptomatic, and diagnosis can be made clinically or serologically.
Am J Med. 1986 Jul;81(1):153-7.
Rocky Mountain spotted fever presenting as thrombotic thrombocytopenic purpura.
Turner RC, Chaplinski TJ, Adams HG.
Abstract
A patient presented with findings compatible with thrombotic thrombocytopenic purpura. The diagnosis of Rocky Mountain spotted fever was also considered because the patient was a hunter in a tick-infested area. He was treated for both diagnoses. The patient recovered and a diagnosis of Rocky Mountain spotted fever was confirmed by serologic methods. Clinical symptoms and hematologic parameters of severe Rocky Mountain spotted fever may resemble thrombotic thrombocytopenic purpura, implying that there may be similarities in the pathophysiology of both disorders.
Purpura
Purpura, which is also known as skin hemorrhages and blood spots, is a rash which appears as an outbreak of red dots on the skin. A purpura rash can appear anywhere on the body, but it more commonly appears in specific areas such as the front of the lower legs, or the outer sides of the lower arms.
The direct cause of purpura is blood in the skin which has leaked from blood vessels, which is what makes the little purplish-red dots or blisters to appear.
This bleeding can be the result of several different causes. One common cause is that the platelet count in the bloodstream becomes low enough that bleeding can occur. Another possible explanation is that there is some sort of damage to the blood vessels, which can be exacerbated by fragile or thin blood vessels. It is also possible that some sort of inflammation causes the blood vessels to swell. Ultimately, there are a wide variety of possible explanations for purpura.
In some cases, a spreading rash may be a sign of severe infection, or leukemia, or even meningitis, so a doctor should always be consulted to diagnose the exact cause. Purpura photo, click here.
Tick Borne Disease Related Purpura
Immun Infekt. 1988 Feb;16(1):15-7.
[Schoenlein-Henoch purpura in Borrelia burgdorferi infection]. Schlotfeldt D, Fahrenkrug H. Internistische Praxis, Hamm.
In a 24-year-old patient suffering from recurrent purpura Schoenlein-Henoch, there were found positive Lyme-spirochete IFT. Due to the motion of titres in immune fluorescence examinations the purpura seems to be likely one form of a late manifestation in borrelia infection.
Dtsch Med Wochenschr. 1988 Jul 1;113(26):1061-3.
[Thrombocytopenic purpura caused by Borrelia burgdorferi?].
Schneider T, Lange R, Niederhut D.
Institut für Angewandte Zoologie, Berlin.
In November 1983 a woman born in 1902 was found to have thrombocytopenic purpura with a platelet count of 14,000/microliter. Examination of the sternal marrow resulted in a suspected diagnosis of Werlhof's disease. Platelet counts dropped at times to below 7,000/microliter during immunosuppressive treatment with corticosteroids and azathioprine of three months' duration.
When this treatment was discontinued spontaneous remission occurred until July 1984. Acrodermatitis chronica atrophicans was diagnosed in August 1987. The IgG antibody titre against Borrelia burgdorferi of 1:2,000 in whole blood and the late manifestation of Lyme disease (chronic acrodermatitis atrophicans) suggest a causal relationship with the previous thrombocytopenic purpura.
Klin Padiatr. 1989 Mar-Apr;201(2):133-5.
[Clinical manifestation of Lyme borreliosis in childhood]. Huber A, Baumann W.
Kinderklinik der Johannes Gutenberg-Universität Mainz.
We report on 4 children with different clinical manifestations of Lyme-Borreliosis. One patient presented with a stage 2 typical aseptic meningitis and 2 others with symptoms of Schönlein-Henoch purpura and rheumatic disease respectively.
A further case had bilateral palsy of abducens nerve and unilateral palsy of trochlearis nerve which are described for the first time in Lyme-Borreliosis. Diagnosis was established by detection of specific antibodies to Borrelia in all patients. Differential diagnosis of these symptoms should include Lyme-Borreliosis.
Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1475-81.
Dermatologic manifestations of Lyme disease. Berger BW.
Department of Dermatology, New York University School of Medicine, New York.
Erythema migrams (EM), the distinctive cutaneous lesion of Lyme disease, has a variable clinical appearance, but at some point presents as a centrifugally expanding, usually erythematous, annular patch. Of 237 patients with this condition, 201 (85%) were examined initially from May through September.
Thirty-four (14%) remembered having been bitten by a deer tick. The median interval from the bite to the appearance of EM was 9 days (range, 1-36 days). Forty-one (17%) of the patients had multiple EM lesions.
Of the 237 patients, 128 (54%) manifested major extracutaneous signs and symptoms. Although EM also has a variable histologic picture, the presence of a deep and superficial perivascular and interstitial lymphohistiocytic infiltrate containing plasma cells is diagnostic.
Spirochetes can be demonstrated with Warthin-Starry staining in approximately 40% of the biopsy specimens. Concomitant cutaneous lesions appeared on some patients before and during antibiotic therapy.
Nine patients with serologic evidence of Borrelia burgdorferi infection had cutaneous lesions other than EM, including granuloma annulare (three), erythema nodosum (two), papular urticaria (two), Henoch-Schönlein-like purpura (one), and morphea (one). Whether these entities are cutaneous markers of Lyme disease or are coincidental findings is yet to be determined.
Hautarzt. 1991 Jun;42(6):356-65.
[Borrelia infections of the skin--progress of knowledge since the discovery of Lyme disease]. Garbe C.
Universitäts-Hautklinik und Poliklinik, Klinikum Steglitz Freien Universität Berlin.
The description of Lyme disease in 1976 and the detection of its causative agent, the spirochete Borrelia burgdorferi (B. burgdorferi), in 1982 led to an increase in our knowledge of the course of B. burgdorferi infection and its clinical manifestations.
The classic tick-borne dermatoses erythema chronicum migrans (ECM), lymphadenosis benigna cutis (LABC) and acrodermatitis chronica atrophicans (ACA) were proven by isolation of the spirochete from skin lesions to be caused by B. burgdorferi infection.
In early disease (less than 1 year) ECM and LABC can develop locally at the site of infection (stage I), but both these skin manifestations can also occur together with multiple lesions after dissemination of the causative organism (stage II). ACA is typical for late infection (greater than 1 year, stage III).
High titres of B. burgdorferi antibodies have been found in patients with localized sclerodermalike lesions (circumscribed scleroderma, lichen sclerosus et atrophicus, anetoderma), and frequent simultaneous occurrence of ACA suggests an association with late B. burgdorferi infection.
Similarly, we found four cases of cutaneous B-cell lymphoma possibly arising from LABC in association with the same markers of late B. burgdorferi infection.
Additionally, some cases of Schönlein-Henoch purpura and of Shulman syndrome may be associated with Lyme borreliosis. The disease is endemic in central Europe, and almost exclusively ticks of the Ixodes ricinus complex seem to transmit B. burgdorferi to humans, whereas the reservoir of infection seem to be rodents, especially mice.
The main diagnostic tool is serological examination for B. burgdorferi antibodies, which will become detectable 3-6 weeks after infection. Enzyme-linked immunosorbent assay (ELISA) and the indirect immunofluorescence test (IFT) revealed similar sensitivity.
In early disease, sensitivity for antibody detection could be improved by immunoblot technique and by flagellum-ELISA, which is specific for this early sensitizing B. burgdorferi antigen. For treatments, penicillin is no longer recommended as the drug of first choice, because low sensitivity of B. burgdorferi has been observed in vitro and in vivo. Tetracycline, doxycycline and amoxicillin p.o. are now preferred for the treatment of Lyme borreliosis, and in neurologic and cardiac abnormalities ceftriaxone i.v. is recommended. Treatment duration should be 14 days in early disease and 30 days in late disease.
Am J Hematol. 1995 Sep;50(1):72-3.
Thrombotic thrombocytopenic purpura (TTP) associated with a Borrelia burgdorferi infection. Schröder S, Spyridopoulos I, König J, Jaschonek KG, Luft D, Seif FJ.
Infez Med. 2008 Jun;16(2):99-102.
Immune thrombocytopenic purpura as a complication of Bartonella henselae infection. Palumbo E, Sodini F, Boscarelli G, Nasca G, Branchi M, Pellegrini G.
Dipartimento di Pediatria, Ospedale di Sondrio, Sondrio, Italy.
Immune thrombocytopenic purpura is an infrequent yet well-recognized complication of viral infections, such as mumps, rubella, varicella, cytomegalovirus, parvovirus and infectious monunucleosis by Epstein-Barr virus.
Some recent studies have described a possible association between Henoch-Schonlein purpura, a non-thrombocytopenic purpura, and seropositivity for Bartonella henselae, but in the literature only sporadic case reports have described a severe immune thrombocytopenic purpura as a complication of Bartonella henselae infection.
We report a case of an immunocompetent child with clinical and serological evidence of Bartonella henselae infection presenting with purpura and cervical lymphoadenopathy and treated with intravenous immunoglobulin. The patient obtained a rapid and persistent increase in platelet count and a complete regression of purpura.
Cardiology. 2009;114(3):208-11. Epub 2009 Jul 15.
Infective endocarditis by Bartonella quintana masquerading as antineutrophil cytoplasmic antibody-associated small vessel vasculitis. Sugiyama H, Sahara M, Imai Y, Ono M, Okamoto K, Kikuchi K, Nagai R.
Department of Cardiovascular Medicine, University of Tokyo Hospital, Tokyo, Japan. hsugiyama-tky@umin.ac.jp
The Bartonella species have been recently recognized as important causative agents of culture-negative bacterial endocarditis. Antineutrophil cytoplasmic antibodies (ANCAs) have been associated with the spectrum of idiopathic small vessel vasculitis.
However, a variety of infections can result in a false-positive ANCA test, and especially subacute bacterial endocarditis (SBE) with the presence of ANCAs occasionally mimics the clinical manifestations of an ANCA-associated vasculitis such as skin purpura and glomerulonephritis. In contrast, noninfectious endocardial involvement is known to be part of the spectrum of the manifestations of the ANCA-associated vasculitis.
Therefore, it is crucial to distinguish an ANCA-positive SBE from an ANCA-associated vasculitis with endocardial compromise, because the misdiagnosis of an SBE as an ANCA-associated vasculitis can lead to an inappropriate immunosuppressive therapy with catastrophic consequences. The differential diagnosis is sometimes difficult, especially in the case of culture-negative infective endocarditis with a positive ANCA test.
We describe here a case of a culture-negative SBE caused by Bartonellaquintana, accompanied with a positive cytoplasmic ANCA test and clinical findings masquerading as ANCA-associated vasculitis. Both a serological test for Bartonella and polymerase chain reaction restriction fragment length polymorphism analysis were helpful for a correct diagnosis and appropriate treatment.
BMC Infect Dis. 2005 Apr 5;5:21.
Bartonella seropositivity in children with Henoch-Schonlein purpura. Robinson JL, Spady DW, Prasad E, McColl D, Artsob H.
Department of Pediatrics and Stollery Children's Hospital, University of Alberta, Edmonton AB, Canada. jr3@ualberta.ca
BACKGROUND:
An association between Henoch-Schonlein purpura (HSP) and seropositivity for Bartonella henselae (BH) has been described. The objective of this study was to see if such an association exists in northern Alberta.
METHODS:
Immunofluorescent antibody testing utilizing an antigen prepared from B. henselae was undertaken on sera from six children with current HSP, 22 children with remote HSP, and 28 controls that were matched for age. Blood from the six children with current HSP was analysed by polymerase chain reaction (PCR) assay with primers derived from the citrate synthase (gltA) gene for the detection of Bartonella DNA.
RESULTS:
The seropositivity rate for BH was 61% in cases versus 21% in controls (p < 0.03). The PCR assay was negative in all six current cases.
CONCLUSION:
There is an increased seropositivity rate for BH in children with HSP. However, it is not clear if infection with B. henselae or a related Bartonella species can result in HSP, or if the increased seropositivity is from non-specific or cross-reacting antibodies.
MedGenMed. 2007 Sep 13;9(3):54.
Do bartonella infections cause agitation, panic disorder, and treatment-resistant depression? Schaller JL, Burkland GA, Langhoff PJ.
Professional Medical Services of Naples, Naples and Tampa, Florida, USA. jschaller@embarqmail.com
INTRODUCTION:
Bartonella is an emerging infection found in cities, suburbs, and rural locations. Routine national labs offer testing for only 2 species, but at least 9 have been discovered as human infections within the last 15 years. Some authors discuss Bartonella cases having atypical presentations, with serious morbidity considered uncharacteristic of more routine Bartonella infections.
Some atypical findings include distortion of vision, abdominal pain, severe liver and spleen tissue abnormalities, thrombocytopenic purpura, bone infection, arthritis, abscesses, heart tissue and heart valve problems. While some articles discuss Bartonella as a cause of neurologic illnesses, psychiatric illnesses have received limited attention.
Case reports usually do not focus on psychiatric symptoms and typically only as incidental comorbid findings. In this article, we discuss patients exhibiting new-onset agitation, panic attacks, and treatment-resistant depression, all of which may be attributed to Bartonella.
METHODS:
Three patients receiving care in an outpatient clinical setting developed acute onset personality changes and agitation, depression, and panic attacks. They were retrospectively examined for evidence of Bartonella infections. The medical and psychiatric treatment progress of each patient was tracked until both were significantly resolved and the Bartonella was cured.
RESULTS:
The patients generally seemed to require higher dosing of antidepressants, benzodiazepines, or antipsychotics in order to function normally. Doses were reduced following antibiotic treatment and as the presumed signs of Bartonella infection remitted. All patients improved significantly following treatment and returned to their previously healthy or near-normal baseline mental health status.
DISCUSSION:
New Bartonella species are emerging as human infections. Most do not have antibody or polymerase chain reaction (PCR) diagnostic testing at this time. Manual differential examinations are of unknown utility, due to many factors such as low numbers of infected red blood cells, the small size of the infecting bacteria, uncertainty of current techniques in viewing such small bacteria, and limited experience.
As an emerging infection, it is unknown whether Bartonella occurrence in humans worldwide is rare or common, without further information from epidemiology, microbiology, pathology, and treatment outcomes research.
CONCLUSION:
Three patients presented with acute psychiatric disorders associated with Bartonella-like signs and symptoms. Each had clear exposure to ticks or fleas and presented with physical symptoms consistent with Bartonella, eg, an enlarged lymph node near an Ixodes tick bite and bacillary angiomatosis found only in Bartonella infections.
Laboratory findings and the overall general course of the illnesses seemed consistent with Bartonella infection. The authors are not reporting that these patients offer certain proof of Bartonella infection, but we hope to raise the possibility that patients infected with Bartonella can have a variety of mental health symptoms.
Since Bartonella can clearly cause neurologic disorders, we feel the presence of psychiatric disorders is a reasonable expectation.
Transfusion. 2008 Feb;48(2):349-57. Epub 2007 Nov 19.
Twice-daily plasma exchange for patients with refractory thrombotic thrombocytopenic purpura: the experience of the Oklahoma Registry, 1989 through 2006. Nguyen L, Li X, Duvall D, Terrell DR, Vesely SK, George JN.
Department of Biostatistics and Epidemiology, College of Public Health, The University of Oklahoma Health Science Center, Oklahoma City, OK 73190, USA.
BACKGROUND:
Twice-daily plasma exchange has been used for patients with thrombotic thrombocytopenic purpura (TTP) who are unresponsive to treatment with daily plasma exchange for many years but with no clear evidence of effectiveness.
STUDY DESIGN AND METHODS:
The 18 years' experience of The Oklahoma TTP-HUS (hemolytic-uremic syndrome) Registry, 1989 through 2006, with twice-daily plasma exchange for 31 episodes of TTP in 28 patients is reported. A definite response to twice-daily plasma exchange was defined a priori as a platelet (PLT) count increase after twice-daily plasma exchange on two separate occasions during the treatment of a single episode of TTP, with no change of other treatments.
A possible response was defined as a PLT count increase after initiation of twice-daily plasma exchange only once with or without change of other treatments.
RESULTS:
A definite response to twice-daily plasma exchange occurred in 3 episodes (three patients), 27 episodes had a possible response, and 1 episode had no response. The three patients with a definite response had ADAMTS13 activities of 5, 6, and 12 percent and all had an inhibitor; the patient with no response was subsequently determined to have Rocky Mountain spotted fever.
CONCLUSION:
Twice-daily plasma exchange was typically considered in acutely ill patients who had initially responded but then severe thrombocytopenia recurred, often with new neurologic abnormalities, while continuing daily plasma exchange. In three patients, twice-daily plasma exchange appeared to be beneficial. In most patients, a benefit of twice-daily plasma exchange could not be clearly documented because other treatments were initiated or intensified.
Clin Pediatr (Phila). 2002 Mar;41(2):117-8. Severe thrombocytopenic purpura as a complication of cat scratch disease. Borker A, Gardner R. LSU Health Sciences Center and Childrens Hospital of New Orleans, LA 70118, USA.
Lancet. 1997 Nov 29;350(9091):1602. Bartonella-like erythrocyte inclusions in thrombotic thrombocytopenic purpura. Tarantolo SR, Landmark JD, Iwen PC, Kessinger A, Chan WC, Hinrichs SH.