Mycobacterial Skin Infections Research Articles

The fish tank strikes again: Metachronous nontuberculous mycobacterial skin infection in an immunosuppressed host

An 82-year-old woman on long-term prednisolone for chronic obstructive airways disease presented with a 2-month history of nodules on her left forearm. This occurred 10 years after nodules on her right forearm caused by a culture-proven Mycobacterium marinum infection. Histopathological examination, polymerase chain reaction and culture of biopsy specimens were positive for M. chelonae. To our knowledge this is the first case of metachronous nontuberculous mycobacterial skin infection reported, and it highlights the diagnostic and therapeutic challenges of such infections.

Systematic review of tattoo-associated skin infection with rapidly growing mycobacteria and public health investigation of a cluster in Scotland, 2010

Sporadic cases and outbreaks of tattoo-associated skin infection with rapidly growing mycobacteria have been reported although they often contain few details of public health investigations and have not previously been systematically collated. We present the details of the public health investigation of a cluster of cases, which occurred in Scotland in 2010. Investigation of the cluster involved case finding, environmental investigation of the tattoo studio and pathological and microbiological investigation of possible cases and tattoo ink. Mycobacterium chelonae was isolated from one case and three probable cases were identified. M. chelonae was grown from an opened bottle of ink sourced from the studio these cases had attended. In addition, in order to identify all published cases, we conducted a systematic review of all reported cases of tattoo-associated skin infection with rapidly growing mycobacteria. A total of 25 reports were identified, describing 71 confirmed and 71 probable cases. Mycobacteria were isolated in 71 cases and M. chelonae was cultured from 48 of these. The most frequently postulated cause of infection was the dilution of black ink with tap water. Reports of tattoo-associated rapidly growing mycobacterial skin infection are increasing in frequency. Interested agencies must work with the tattoo industry to reduce the risk of contamination during tattoo ink manufacture, distribution and application.

BCG-treated M2-macrophages enhance IFN-γ production of T cells (P3348)

Abstract M1- and M2-polarized Macrophage (MΦ) subtypes differentially regulate anti-mycobacterial defense. To examine their roles in human infection, we compared the gene expression profile of M1- vs. M2-MΦ to the expression profile of lesional skin from patients with restricted (tuberculoid, T-lep) vs. disseminated (lepromatous, L-lep) leprosy (a mycobacterial skin infection). Rank-Rank Hypergeometric Overlap (RRHO) is a novel algorithm for comparing full gene expression profiles from two independent microarray experiments that generates the most statistically significant overlapping gene list without requiring strict p-value/fold change cutoffs. RRHO analysis showed significant overlap of genes between M2-MΦ and L-lep lesions (n = 1559, max log hypergeometric p-value = 196), indicating a role for M2-MΦ in immune unresponsiveness. Bacillus Calmette-Guerin (BCG) is given to protect household contacts against leprosy. We hypothesized that BCG treatment may affect the function of M2-MΦ and investigated its effects in vitro. We found that BCG-treated M2-MΦ secreted less IL-10 (p < 0.05), with no effect on IL-12p40, compared to untreated M2-MΦ. In addition, BCG-treated M2-MΦ increased the frequency of IFN-γ producing cells in an antigen non-specific manner (p < 0.05), suggesting an adjuvant effect of BCG. Our data indicates M2-MΦ can be reprogrammed by BCG, resulting in increased IFN-γ production to enhance anti-mycobacterial immunity.

Detection of mycobacterial skin infections by polymerase chain reaction (PCR) amplification of deoxyribonucleic acid (DNA) isolated from paraffin-embeded tissue

Atypic mycobacterial granulomatous skin infections are often caused by Mycobacterium marinum, Mycobacterium ulcerans, Mycobacterium fortuitum, Mycobacterium chelonae, and rarely Mycobacterium avium. The lesions appear as papules, nodules in hands, plaque blisters, wart ulcers and markers transmission (sporotrichosis) in the path of lymph glands and lesions; and display a granulomatous accumulation of giant cells. Infection is limited to the skin, and in other cases it could lead to immunosuppression. To determine if mycobacteria were present in granulomatose skin lesion, a total of 58 paraffine tissue blocks were obtained and deoxyribonucleic acid (DNA) isolated the polymerase chain reaction (PCR) that was used to amplify the 16S rRNA gene. PCR amplification demonstrated the presence of Mycobacterium spp. in 18 blocks (31%). Among these 18 blocks, 8 (44%) positive for M. marinum, 33 (17%) for M. ulcerans, 5 isolates (27%) M. fortuitum and M. chelonae, 2 (12%) M. avium. We conclude that mycobacteria ought to be considered in the treatment of skin granulomas in Iran. Key words: Mycobacterial, granuloma skin infection, polymerase chain reaction (PCR).

Tropical bacterial infections

<h3>Aims</h3> To describe bacterial infections that are overrepresented in Northern Australia. Examples of these would include melioidosis, Q fever, brucellosis, invasive Group A streptococcal infection, non-multiresistant methicillin resistant <i>Staphylococcus aureus</i> (nmMRSA) soft tissue infections, atypical mycobacterial skin infections and leptospirosis. <h3>Methods</h3> A review of the epidemiology, risk factors, clinical features and laboratory diagnosis of the above. <h3>Results</h3> The possibility of acquiring one of a range of micro-biologically fascinating infections is one of the risks of visiting or living in tropical Northern Australia. A variety of factors affect this end result and include rainfall, soil, co-morbidities and native mammals. The early culture of appropriate clinical material remains the mainstay of diagnosis for most of these. Serology, with its limitations in some instances, is still the major diagnostic modality for Q fever and leptosirosis. Molecular diagnostics currently has a limited place. <h3>Conclusions</h3> Visitors to Northern Australia are often struck by the spectacular scenery, and lifestyle. This comes at a price though. An awareness of local infectious diseases is essential for all diagnostic laboratories due to the high mobility of the population in general. Early clinical suspicion based on a travel history will ensure appropriate diagnosis and subsequent management.

Non‐tuberculous mycobacterial infections of the skin: A retrospective study of 29 cases

The incidence of infections caused by non-tuberculous mycobacteria has increased in recent years, due to a rise in dermatological procedures and a greater prevalence of immunosuppression in the general population. This study investigated the clinical and microbiological findings of non-tuberculous mycobacterial skin infections. The study population included 29 patients from whom non-tuberculous mycobacteria were cultured after isolation from skin biopsy materials, cutaneous abscesses or exudates. Clinical, microbiological and epidemiological data were collected from each patient. Eight patients were immunocompromised while 21 were not. Precipitating factors such as acupuncture, filler injection, surgical procedures and other traumatic events preceded infection in 13 (including 11 normal hosts and two immunocompromised hosts) of the 29 patients. Multiple skin lesions were present in eight patients (including three normal hosts and five immunocompromised hosts). In eight patients (including four immunocompromised hosts), symptoms were accompanied by tenosynovitis, osteomyelitis and myositis. Mycobacterium abscessus was isolated from nine patients, Mycobacterium fortuitum was isolated from nine patients, Mycobacterium chelonae was isolated from six patients, Mycobacterium marinum was isolated from two patients, a Mycobacterium avium complex member was isolated from two patients, and Mycobacterium haemophilum was isolated from one patient. Ten of the 24 cases caused by rapidly growing organisms (i.e. M. chelonae, M. abscessus and M. fortuitum groups) were precipitated by skin injuries such as acupuncture, filler infection and other medical procedures. Increases in skin medical procedures, including both acupuncture and esthetic interventions, explain the increasing incidence of these organisms. Immunocompromised patients tended to develop multiple skin lesions and deep tissue infections.

Report of oral clarithromycin desensitization

Antibiotic hypersensitivity can lead to significant morbidity, mortality and suboptimal treatment options. Rapid desensitization induces temporary immunological tolerance in a host with type 1 hypersensitivity reaction. We report a case of oral desensitization to clarithromycin. To our knowledge, this is the first protocol published for desensitization to macrolides. A 68-year-old female with a history of giant cell arteritis treated with oral corticosteroids and steroid-induced diabetes presented with small nodules and ulcers on the pre-tibial surface of her legs. Despite multiple courses of oral and parenteral antibiotics for cellulitis, the lesions continued to develop. Skin biopsy of the lesion demonstrated suppurative granuloma formation with acid-fast bacilli on microscopy. The patient reported anaphylaxis to erythromycin 20 years previously and bronchospasm to roxithromycin 5 years previously. She was commenced on rifampicin and moxifloxacin for mycobacterial skin infection, and Mycobacterium chelonaewas subsequently cultured. There was further clinical deterioration and her treatment was changed to doxycycline, intravenous amikacin and intravenous imipenem. Antibiotic susceptibility testing subsequently revealed the isolate was resistant to imipenem, so this was substituted with linezolid. Unfortunately, this was discontinued due to diarrhoea. Intravenous amikacin was not desired as a long-term treatment option due to risk of renal and ototoxicity. Clarithromycin is the treatment of choice for M. chelonae infection [1], but the patient had a strong history of type 1 hypersensitivity with macrolide antibiotics. No published protocol for rapid drug desensitization was available for clarithromycin, so a clarithromycin desensitization protocol was developed (Table 1). The protocol was administered in an intensive care unit with careful observation on a medical ward for 36 h afterwards. No adverse reaction was noted. Table 1 Oral clarithromycin desensitization protocol The patient continued doxycycline and clarithromycin for a total of 18 months. There was an excellent clinical response and no adverse drug reactions were recorded. Serious adverse drug reactions occur in 6.7% of hospitalized patients and rank from the fourth to sixth leading cause of death in these patients [2]. Since 1998 there has been a 2.6-fold increase in serious adverse drug reactions reported to the US Food and Drug Administration [3]. Type 1 (immediate) hypersensitivity reactions occur within minutes to hours of drug administration due to release of vasoactive substances from mast cells and basophils (often IgE-mediated). Clinical manifestations range from urticaria to life-threatening angio-oedema and anaphylaxis. Desensitization procedures were first developed in the 1960s [4]. Rapid desensitization involves incremental exposure to drug antigens at increasing concentrations leading to a therapeutic dose. Antigen-specific mast cell desensitization is thought to be the underlying mechanism for drug desensitization [5]. By inducing temporary clinical and immunological tolerance, patients are able to receive optimal treatment while avoiding or minimizing anaphylaxis and anaphylactoid reactions. Tolerance is maintained only if drug antigens are administered at regular intervals, and repeated desensitizations can also be given [6]. Desensitization protocols have been developed for a variety of drugs including penicillins, cephalosporins, vancomycin, sulfonamides, rifampicin, nonsteroidal anti-inflammatory drugs and chemotherapeutic agents (taxanes, platins). As specific skin prick testing to clarithromycin was not performed in our patient, we cannot be certain that an immediate hypersensitivity reaction would have occurred. However, given her previous immediate hypersensitivity reactions to other 14-membered macrolides erythromycin and roxithromycin, we felt that desensitization to clarithromycin was warranted. Skin prick testing has been well described for penicillins and cephalosporins, and is considered accurate for diagnosing penicillin allergy, as antigenic determinants have been well characterized [7]. Cross-sensitivity within the same antibiotic class is variable, however. There is little information available for diagnostic tests for macrolide allergy, as immediate hypersensitivity reactions are uncommon [8]. A patient in the literature with roxithromycin immediate hypersensitivity demonstrated positive skin prick testing to erythromycin and clarithromycin [9]. These macrolides have a similar chemical structure comprising a 14-membered carbon ring, compared with 15-membered macrolides (azithromycin) and 16-membered macrolides (spiramycin). Use of first-line antibiotics in certain conditions have been shown to have greater efficacy, for example trimethoprim + sulfamethoxazole for Pneumocystis jiroveci pneumonia [10, 11] or penicillin for syphilis, especially in HIV-infected individuals [12]. Macrolide antibiotics have an important role in the treatment of nontuberculous mycobacterial infections [13]. In our case report clarithromycin was a desirable treatment option, and rapid oral desensitization to clarithromycin was successful with no adverse events reported. We believe this is the first published protocol for desensitization to macrolide antibiotics and anticipate that its use can be extended to other centres worldwide.

Delayed diagnosis of atypical mycobacterial skin and soft tissue infections in non-immunocompromized hosts

Relapsing or persisting skin and soft tissue infections after injury with biological materials should prompt consideration of atypical mycobacteria, even in non-immunocompromized hosts. We report 3 cases where diagnosis was delayed for 3-10 months. Insidiously, Mycobacterium marinum infection can occur without any contact to fish tank or swimming pool.

Application of Real-time PCR to Recognize Atypical Mycobacteria in Archival Skin Biopsies

Atypical mycobacterial skin infections are difficult to diagnose owing to their aspecific histopathologic presentations and to the presence of few bacteria. Therefore, these infections are often not recognized. Molecular detection of mycobacterial DNA has proven to be useful in clinical samples. The aim of this study was to investigate the incidence of mycobacterial involvement in skin biopsies showing granulomatous inflammation, using real-time polymerase chain reaction (PCR). Real-time PCR specific for the genus Mycobacterium and the species Mycobacterium avium and Mycobacterium haemophilum was performed on formalin-fixed/paraffin-embedded biopsies from patients with granulomatous inflammation of the skin, from the period 1984 to 2004. A control group was assembled from patients with proven basal cell carcinoma. Amplicons of all positive reactions were sequenced to confirm or identify the mycobacterial species. Of 30 patients, 13 (43%) were found to be positive for mycobacterial infection, of whom only 5 patients had been previously diagnosed with a mycobacterial disease. M. haemophilum was identified as the most common species (n=7). The other identified species were Mycobacterium malmoense, Mycobacterium gordonae, and Mycobacterium marinum. The results show that real-time PCR is useful in detecting mycobacterial infections in undiagnosed formalin-fixed/paraffin-embedded skin samples and that the application of molecular approaches would improve the diagnoses of mycobacterial skin infections.

Identification of Mycobacterium marinum 65 kD heat shock protein gene by polymerase chain reaction restriction analysis from lesions of swimming pool granuloma

Nontuberculous mycobacterium (NTM) had been reported to cause cutaneous infections which are difficult to interpret due to the variability of the clinical manifestations. Among NTM infections, Mycobacterium marinum (M. marinum) are mostly seen to cause skin infection. It is therefore important to establish a rapid approach for detection and identification of M. marinum from lesions of patients with suspected M. marinum infections. Specimens were obtained from 5 patients with swimming pool granuloma. DNA was extracted and polymerase chain reaction (PCR) was performed. PCR products were digested with Hae III and BstE II, then analysed by pattern restriction analysis to detect heat shock protein (hsp) 65 kD gene. The 65 kD hsp gene was found in all specimens from patients with swimming pool granuloma. PCR restriction analysis (PRA) identified all 5 samples to be M. marinum infections, and the result was consistent with that of routine bacteriological identification. The lesions subsided or markedly improved upon treatment. PRA is a sensitive, specific and rapid method in identification of mycobacteria. Application of this method will be helpful for early diagnosis of mycobacterial skin infections.

Successful Treatment of Localized Cutaneous Infection Caused by Mycobacterium scrofulaceum with Clarithromycin

Cutaneous infection arising from Mycobacterium scrofulaceum, a nontuberculous mycobacteria, has rarely been reported, and most of the reported infections were disseminated forms in patients with AIDS or other immunocompromising illness. We describe an occurrence of localized mycobacterial skin infection caused by M. scrofulaceum in a previously healthy child that manifested as a red nodule on the cheek. A biopsy specimen of the lesion demonstrated granulomatous infiltration in the dermis. M. scrofulaceum was isolated from culture of a tissue specimen. Polymerase chain reaction amplified specific fragments for M. scrofulaceum. The patient was treated successfully with clarithromycin as monotherapy for 6 months, leading to complete healing without recurrence during a follow-up period of 2 years.

Leproid granulomas: a unique mycobacterial infection of dogs

In 1973, a Rhodesian veterinarian, Richard Smith, documented a mycobacterial skin infection in a Doberman and a Rhodesian Ridgeback dog that was characterised by variably sized subcutaneous nodules. It was thought at first that these dogs may have had tuberculosis and, because of public health considerations, they were euthanased and subjected to postmortem examination. There was no internal organ involvement at necropsy and, although acid-fast bacilli (AFB) were abundant in the lesions, culture was negative for the tubercle bacillus. Similar cases were recorded soon thereafter in an Australian veterinary discussion forum, although the infection was not subjected to systematic investigation until the end of the 20th century. The disease was given the name ?canine leprosy? by some veterinary dermatologists, but the alternative name canine leproid granuloma syndrome (CLGS) was later suggested by an Australian veterinarian David Watson. It is now clear that leproid granulomas are not uncommon and indeed are by far the most frequently encountered mycobacterial disease of dogs in Australia.

Case report: MR features of granulomatous myositis

A 51-year-old woman with a 23-year history of systemic lupus erythematosus (SLE), on long-term low-dose steroids, presented with right thigh swelling and erythema of 2-weeks duration. She was afebrile and denied antecedent trauma or injection. Relevant past history included right caphalic vein thrombosis; and culture and biopsy proven cutaneous tuberculous granulomas of the right forearm 3 years ago, which responded to a 9-month regimen of rifampicin, isoniazid and ethambutol. The WBC count was 13.8 x 109/1 with granulocytosis (92%) and lymphopenia (690//zl). Serum creatinine phosphokinase (1211 u/l) and aldolase (32.4u/1) levels were elevated. Doppler study of the right lower limb excluded a deep vein thrombosis. Magnetic resonance (1.5 T) images showed subcutaneous oedema and abnormal signal intensity in the quadriceps femoris. On Tl-weighted (SE 600/17) images, the swollen muscles were slightly hyperintense to normal muscle with loss of inter-muscular planes (Figs la & 2a). These areas enhanced moderately following intravenous gadolinium-DTPA and were hyperintense on the T2-weighted (FSE 4000/102) images (Figs lb & 2b). Fast multiplanar inversion recovery (FMPIR 3000/102) (Fig. 2c) accentuated the abnormalities. These signal and enhancement characteristics suggested myositis. No bony abnormality was detected. Open muscle biopsy of the abnormal rectus femoris and vastus intermedialis muscles revealed granulomatous myositis, with extensive myocyte necrosis surrounded by epitheloid histiocytes, multinucleated giant cells and lymphocytes. There was no evidence of acid fast bacilli (AFB), fungus or vasculitis. The tissue and blood cultures were also sterile. The patient did not receive specific therapy for her thigh swelling and was discharged. Shortly after, dusky erythematous plaques and nodules in a sporotrichoid distribution erupted predominantly in the swollen right lower limb. The dermatologist's clinical diagnosis was an atypical mycobacterial skin infection. Skin biopsy showed granulomas with caseous necrosis and AFB, but cultures for mycobacteria were negative. Very rapid clinical response to empirical treatment with clarithromycin and ciprofloxacin for atypical mycobacterial infection ensued. After 3 months, treatrnent was ceased for suspected antibiotic-induced purpura (subsequently found to be caused by NSAIDs). Within 2 weeks, the lesions relapsed. Repeat skin biopsies all confirmed cutaneous tuberculous infection. Multiple cultures for mycobacteria from skin specimens, sputum and laryngeal swabs were negative. The chest radiograph was normal and MRI of the himbosacral spine excluded vertebral osteomyelitis. Resumption of the antibiotics, reinforced with ethambutol, isoniazid and rifampicin, finally saw gradual resolution of the right thigh swelling and skin lesions., On the follow-up MR imaging, 8 months from commencement of therapy, there was significant resolution of the abnormal signals in the right thigh (Fig. 3). literature search (Medline: 1976-March 1995), but none of atypical mycobacterial myositis. Our patient was proven on multiple skin biopsies to have cutaneous mycobacterial infection, and the clinical picture was that of atypical mycobacteria. The granulomatous myositis diagnosed on biopsy 1 month before the onset of the cutaneous lesions was also mycobacterial in origin, as there was resolution, clinically and on repeat MRI, following anti-tuberculous therapy. Pyogenic myositis, caused by Staphylococcus aureus in more than 90% of cases [5], is endemic in the tropics where it accounts for 4% of surgical admissions [6]. It occurs infrequently in the temperate climates, but has been increasingly reported in North America and Europe. It affects all ages, and typically involves a single large muscle group, usually the thigh (quadriceps femoris), although multiple muscle involvement is found in 12% to 43% [7]. It is associated with trauma (in 20% to 50% of cases), a history of travel to the tropics, nutritional deficiencies, underlying parasitic or occult viral myositis, and immunocompromised states. These include diabetes mellitus, infection with human immunodeficiency virus, leucopenia with leukaemia, Felty's syndrome, rheumatoid arthritis, and progressive systemic sclerosis [8]. We are unaware of any case previously reported in an SLE patient. Corticosteroid therapy

Non‐tuberculous mycobacterial skin infections

AbstractGeneral description The mycobacteria are a large genus which includes important pathogens of man and other vertebrates, apparently harmless commensals, and free‐living saprophytes. The relative importance of non‐tuberculous mycobacterial diseases has been undergoing evolution during the past few years and further changes and modifications are expected to occur in the near future. In this paper we review the microbiological, clinical, histological and therapeutical aspects of the most important human pathogens of non–tuberculous mycobacteria.Learning objective At the conclusion of this learning activity, participants should be able to describe the pathogenesis. the microbiological, clinical and histological features of non‐tuberculous mycobacterial skin infections and should be able to diagnose and treat these skin diseases.

Fungal and mycobacterial skin infections

Concurrent with the AIDS epidemic has been the resurgence of syphilis to its highest prevalence since the introduction of penicillin in 1943. 1 The popular press has even speculated that syphilis may be the cause of AIDS, an idea clearly dispelled by the isolation of HIV-1 as the causative agent of AIDS. 2 Nonetheless, many clinicians and researchers believe that concurrent infection with both HIV-1 and Treponema pallidum is more than coincidental and that the course of each may be affected by the other. Five clinical observations occur in the course of syphilis in the presence of HIV. 3 These include: 1) the high prevalence of HIV-seropositivity among patients with syphilis; 2) a dysregulation of the antibody response to luetic infection; 3) the rapid progression of syphilis to tertiary stage disease; 4) the inadequacy of benzathine penicillin for the treatment of syphilis in immunocom-promised patients; and 5) the possible vaccination-induced relapse of syphilis.

Nontuberculous Mycobacterial Skin Infections in Two Dogs

Nontuberculous Mycobacterial Skin Infections in Two Dogs

Primary mycobacterial skin infection: A summary.

International Journal of DermatologyVolume 13, Issue 6 p. 353-356 PRIMARY MYCOBACTERIAL SKIN INFECTION: A SUMMARY ROGER A. FELDMAN M.D., Corresponding Author ROGER A. FELDMAN M.D. U. S. Department of Health, Education, and Welfare, Public Health Service, Center for Disease Control, Atlanta, GeorgiaAddress for reprints: Dr. Feldman, Bacterial Diseases Division, Bureau of Epidemiology, Center for Disease Control, Atlanta, Ga. 30333.Search for more papers by this author ROGER A. FELDMAN M.D., Corresponding Author ROGER A. FELDMAN M.D. U. S. Department of Health, Education, and Welfare, Public Health Service, Center for Disease Control, Atlanta, GeorgiaAddress for reprints: Dr. Feldman, Bacterial Diseases Division, Bureau of Epidemiology, Center for Disease Control, Atlanta, Ga. 30333.Search for more papers by this author First published: November 1974 https://doi.org/10.1111/j.1365-4362.1974.tb05067.xCitations: 9AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume13, Issue6November 1974Pages 353-356 RelatedInformation