By Warren R. Heymann, MD
May 1, 2018

 

I met a woman in her early 20’s who is being treated for chronic Lyme disease and Bartonella infections with multiple courses of antibiotics. During my examination, I noted several old white atrophic striae on her hip and leg. Her mother, who was accompanying her, stated matter-of-factly, “Those are due to her Bartonella infection. They started out red.” My response was that striae routinely do that — they are initially red-to-violaceous, prior to turning white.

I listen to my patients — over the years, I have continually learned from them. Even though I was admittedly skeptical, I thought I should examine the current medical literature to determine if Bartonella can cause striae.

Patients with complex medical symptoms including fatigue, headache, poor appetite, in whom a definitive diagnosis cannot be rendered are thought by some to have chronic Lyme disease with coinfections with Anaplasma, Babesia, or Bartonella.

As a dermatologist, I will limit my commentary to striae. I have no doubt that patients’ symptoms are real, however, it must be acknowledged that the concept of these chronic infections is controversial, at best. Lantos and Wormser performed 5 systematic literature searches using Boolean operators and the PubMed search engine. They note it is expected that ticks contain Bartonella DNA — ticks feed on a variety of mammalian hosts that may be reservoirs for Bartonella spp. The presence of Bartonella DNA in the tick does not prove that the tick is a competent vector for transmission to a second mammalian host. They conclude: “The Ixodes spp. ticks that transmit B. burgdorferi are capable vectors of several human pathogens. In all cases, however, these infections produce defined clinical syndromes that are corroborated by objective clinical and laboratory findings. This is true for well-established Babesia-Lyme and Anaplasma-Lyme coinfections…There is little evidence to support tick-borne Bartonella infection or Bartonella-Lyme coinfection.” (1)

The precise pathogenesis of striae is unknown; however, in otherwise healthy individuals, they are thought to occur when excessive stretch overwhelms the dermal integrity of the skin, resulting in a wound‐type response with abnormal and/or incomplete repair. Striae also observed in pregnancy (striae gravidarum, SG), Cushing syndrome, Marfan syndrome, and use of topical steroids. Significant remodeling of dermal elastin fibers with truncation and realignment has been observed. (2). Twenty-eight pregnant women with SG had skin samples biopsied of recently developed, erythematous abdominal lesions that were examined by multiphoton microscopy and immunostaining for protein expression and localization of type I procollagen. Real‐time polymerase chain reaction was used to determine gene expression levels. The authors were able to demonstrate that early SG displays marked separation and disorganized collagen fibrils that fail to form bundles. These alterations may reflect ineffective repair of collagen bundles disrupted by intense skin stretching. Persistent disruption of the collagenous extracellular matrix likely promotes formation and atrophy of SG. (3) Additionally, estrogen receptor has been demonstrated to be upregulated in affected skin, suggesting a role for hormonal influences in the development of the lesion. (2)

My PubMed search of the literature for histologic evidence of striae and Bartonella yielded one case: an 18-year-old man with illness of three-year duration, whose symptoms included: fatigue, headaches, and fine tremors. His physical examination demonstrated red conjunctivae, cervical lymphadenopathy, and erythematous striae involving both legs and the buttock. Histopathology of the right deltoid skin lesion contained features of a blue nevus. The striae lesional biopsy from the left thigh contained minimal nonspecific superficial perivascular chronic inflammation. Immunostaining of the striae tissue from the son’s skin biopsy revealed B. henselae immuno-positive staining within the dermis and by confocal microscopy imaging, the bacteria were external to vascular tissue. DNA was amplified and successfully sequenced from the striae biopsy sample. Bartonella spp. DNA was not amplified from the biopsy of his blue nevus. (4)

Even if confirmed by other studies, an association does not equate with causation – this was not a fulfillment of Koch’s postulates. The fact that the organism is not present in his blue nevus does not imply pathogenesis where it is found. Clearly his striae were in an inflammatory stage; the blue nevus (presumably) was not. Perhaps the inflammation alone could have predisposed a tissue affinity for the organism, which could be an innocent bystander.

Boozalis et al performed a study of 12 boys (11 to 17 years old) with horizontal striae distensae (SD) of the lower back, by telephone surveys and medical chart reviews. The impetus for the study was based on “common concerns that these boys were using unmonitored exogenous steroids, had a metabolic condition, or were infected with Bartonella henselae (cat‐scratch disease) or Borrelia burgdorferi (Lyme disease).” In their retrospective review, titers for B. henselae and borreliosis were only determined in one of the patients before he was referred to pediatric dermatology, which limited their ability to exclude the possibility of infection as the trigger for SD. [There was no serologic evidence of infection.] None of the boys had a history of unmonitored injectable or oral anabolic steroid use. The authors concluded that horizontal SD of the lower back in adolescent boys is associated with rapid growth spurts, tall stature, and a positive family history of SD. This suggested that SD are a normal physiological process in growing adolescent boys rather than a sign of underlying pathology. (5)

In conclusion, there is not enough data to completely rule out the theory that rare cases of striae may be caused by Bartonella infection. I surmise that he answer could be determined by inoculation of Bartonella in appropriate animal model. Based on the current literature any pathogenic association of Bartonella with striae is a real stretch.

1. Lantos PM, Wormser GP. Chronic coinfections in patients diagnosed with chronic Lyme disease. A systematic review. Am J Med 2014; 127: 1105-10.
2. Sambi P, Watson REB. Cause or consequence? Identification of collagen remodelling in striae. Br J Dermatol 2018; 178: 590-1.
3. Wang F, et al. Severe disruption and disorganization of dermal collagen fibrils in early striae gravidarum. Br J Dermatol 2018; 178: 749-60.
4. Maggi RG, et al. Bartonella henselae bacteremia in a mother and son potentially associated with tick exposure. Parasit Vectors 2013; 6: 101.
5. Boozalis E, et al. Demographic characteristics of teenage boys with horizontal striae distensae of the lower back. Pediatr Dermatol 2018; 35: 59-63.

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