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Alert Number 241

Lyme Disease and CLL

Date: July 14, 2007

It is that time of the year: time of picnics, walks through woods, playing Frisbee with the kids in the back-yard. And it is the time of the year when Lyme disease becomes a concern, especially for people living in areas where this disease is pretty well entrenched in the wild animal population. Got deer in your neighborhood? Chances are there are lots of deer ticks around, infected with Lyme.

There has been tons of stuff written about Lyme disease. This is the most common tick borne disease in the United States. It is caused by the bacterium Borrelia burgdorferi, carried by a tick that infests animal populations. The rash associated with a tick bite is a circular to oval red patch occurring at the site of the tick bite. The tick requires 24 hours to drink its fill of your blood, during which time the Lyme spirochetes multiply in its gut, and they are then secreted into its saliva and therefore into you. Typically the rash occurs within a few days to weeks following the bite. The “bulls-eye” is often larger than 10 cm or more and this is highly suggestive of the disease. Prime time for infection is between April and October.

Secondary rash can occurs in 17-50% of patients. The skin eruptions may occur in bunches, sometimes as many as 80 or more splotches, scattered over the entire body. In some European varieties of this nasty bacteria, the rash may occur as a solitary, nonexpanding, persistent bluish-red plaque or nodule, measuring a few centimeters. What makes Lyme disease so nasty is that it can linger for months and years following the initial attack. Chronic and often very painful arthritis, and chronic fatigue are common adverse effects. A friend of mine had this nasty disease – not a pretty sight.

The reason why I am writing about this is that in just the last 2 weeks I heard from three of our members asking about the special implications of Lyme disease in our patient community. By now you should know that CLL patients can have way over the top response to bug bites. Lyme is no exception. As the abstracts below show, it is shown that you can have skin infiltration of the CLL at the site of the Lyme infection. More worrisome, there are links between Lyme disease and a variety of lymphomas, including marginal zone lymphoma. Lyme infection is also known to make skin cancer issues much worse.

Here is my take on the whole thing. Prevention is a whole lot better than hassling with controlling the problem after infection has set in. You do not want to have to deal with Lyme on top of the CLL monkey you already have on your back. Take precautions folks. Commonsense is a wonderfully effective therapy regimen.

A couple of housekeeping issues:

  1. Please, make sure your email filters are not set to reject mail from us as spam. I will not be able to send you the full text articles you request if I get blocked by your software.
  2. Second, PC is doing just fine! Please do not feel you have to worry or hesitate about writing me. The whole point of the Battle plan is to implement therapy at a time of our choosing. PC is in fine fettle, ready to battle the disease and everything else. Frankly, he is running me ragged and I don’t even have CLL.
  3. Third, we suspended fund-raising because we have met our goals, and we do not believe in wheedling money out of our members for the sheer sake of getting more money. If and when we come up with good clinical trials that deserve your financial support, we will let you know. Until then, the money belongs in your wallets - darn it, it is your money.

Be well,



J Cutan Pathol. 2002 Mar;29(3):142-7.

Specific cutaneous infiltrates of B-cell chronic lymphocytic leukemia (B-CLL) at sites typical for Borrelia burgdorferi infection.

Cerroni L, Höfler G, Bäck B, Wolf P, Maier G, Kerl H.

Department of Dermatology, University of Graz, Austria.

BACKGROUND: Cutaneous manifestations of B-cell chronic lymphocytic leukemia (B-CLL) comprise a wide spectrum of clinicopathologic presentations. In some cases, onset of skin lesions is triggered by antigenic stimulation, and specific skin infiltrates at sites of previous herpes simplex or herpes zoster infection have been well documented. Specific skin manifestations of B-CLL can also be observed at sites typical for lymphadenosis benigna cutis (nipple, scrotum, earlobe), a Borrelia burgdorferi-associated cutaneous B-cell pseudolymphoma.
METHODS: We studied specific skin manifestations of B-CLL arising at sites typical for B. burgdorferi-induced lymphadenosis benigna cutis, analyzing tissues for presence of B. burgdorferi DNA using the polymerase chain reaction (PCR) technique. Six patients with B-CLL (M : F = 4 : 2; mean age: 67.8) presented with specific skin lesions located on the nipple (four cases) and scrotum (two cases).
RESULTS: Clinically there were solitary erythematous plaques or nodules. Histology revealed in all cases a dense, monomorphous infiltrate of small lymphocytes showing an aberrant CD20+/CD43+ phenotype. In all cases monoclonality was demonstrated by PCR analysis of the JH gene rearrangement. PCR analysis showed in four of the six cases the presence of DNA sequences specific for B.burgdorferi.
CONCLUSIONS: Our study demonstrates that infection with B. burgdorferi can trigger the development of specific cutaneous infiltrates in patients with B-CLL.

PMID: 11972710

Borrelia burgdorferi-associated cutaneous marginal zone lymphoma: a clinicopathological study of two cases illustrating the temporal progression of B. burgdorferi-associated B-cell proliferation in the skin.

Goodlad JR, Davidson MM, Hollowood K, Batstone P, Ho-Yen DO.

Department of Pathology, Raigmore Hospital, Inverness, UK.

AIMS: A relationship between Borrelia burgdorferi and primary cutaneous B-cell lymphoma (PCBCL) has recently been confirmed following demonstration of the organism in lesional skin of patients with PCBCL. We report herein two cases of B. burgdorferi-associated PCBCL which strengthen this association by demonstrating the organism in cutaneous B-cell infiltrates present at sites in which PCBCL subsequently developed.
METHODS AND RESULTS: All studies were performed on formalin-fixed paraffin-embedded tissues. These were examined by routine light microscopy and immunohistochemically by a standard streptavidin-biotin-complex technique. Genotypic studies were also undertaken using semi-nested polymerase chain reaction (PCR) for immunoglobulin heavy chain gene rearrangement, and nested PCR for B. burgdorferi flagellin gene. Both patients presented with erythematous skin lesions, biopsy of which showed dense perivascular infiltrates comprising small T-lymphocytes and collections of B-blasts. Primary cutaneous marginal zone lymphoma (MZL) developed subsequently in both cases at the same site. PCR for B. burgdorferi flagellin gene was positive in the perivascular lymphocytic infiltrates and the succeeding lymphomas in both patients.
CONCLUSIONS: These results show that, at least in some instances, PCBCL arises from chronically stimulated lymphoid tissue acquired in the skin in response to B. burgdorferi infection. This may have significant therapeutic implications and warrant further studies on the extent of this association.

PMID: 11122431


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