Updated: Jul 13, 2009
Mycobacterium marinum is an atypical Mycobacterium found in salt water and fresh water. M marinum is the most common atypical Mycobacterium to cause infection in humans. Infection occurs following inoculation of a skin abrasion or puncture and manifests as a localized granuloma or sporotrichotic lymphangitis. Diagnosis and treatment are often delayed because of a lack of suspicion for mycobacterial involvement, ie, versus more common bacterial pathogens. Due to the regular use of tumor necrosis factor (TNF) inhibitors for various conditions and immunosuppressants for transplant recipients, infections with mycobacteria other than tuberculosis (MOTT) are increasing.
M marinum infection occurs following trauma to an extremity that is in contact with an aquarium, salt water, or marine animals such as fish or turtles. Exposure to M marinum via swimming pools is rare because most pools are chlorinated.
The pathogen is classified in Runyon group 1 and is a photochromogen, which means it produces yellow pigment when cultured and exposed to light. Culture growth occurs over 7-21 days and is optimal at 25-32°C (77-89.6°F) because the organism is adapted to infect ectotherms, such as fish. Endotherms, such as humans, also can be infected; the cooler extremities are affected more often than central sites. Systemic infection, usually in the context of an immunocompromised host, has been reported. This indicates that the organism is capable of adapting to grow in conditions closer to 37°C.1
After inoculation into the host tissues via an abrasion or other wound, the mycobacteria are phagocytosed by macrophages. Inside the macrophage, they are able to interrupt the formation of the phagolysosome, which would kill the organisms. The mycobacteria then escape the lysosome and can move intracellularly and extracellularly via actin-based motility. This may contribute to cell-to-cell spread.
TNF is important for the immune response against mycobacteria. Studies have demonstrated that in the absence of TNF, macrophages engulf but do not destroy the mycobacteria. Instead, the mycobacteria survive and grow, finally killing the macrophage.2
Studies have revealed 2 pathophysiologically and genetically (ie, via amplified restriction-based polymorphism analysis) distinct populations of M marinum. One group can infect humans and causes acutely lethal disease in fish, while a second group cannot infect humans and causes chronic progressive disease in fish.
Infections caused by M marinum are uncommon but well described in the literature. The estimated annual incidence is 0.27 cases per 100,000 adult patients. Of the approximately 160 cases described, most are case reports of cutaneous infection; however, some have concomitant osteomyelitis, tenosynovitis, arthritis, and/or disseminated infection. Nosocomial infection has never been described.
Infection occurs worldwide, most commonly in individuals with occupational and recreational exposure to fresh or salt water.
M marinum skin infection typically remains localized and does not cause significant morbidity in patients who are immunocompetent. Cases reported in patients who are severely immunocompromised have resulted in disseminated infection involving the bone marrow and viscera and may result in death.
No racial predilection is apparent for M marinum skin infection.
No sexual predilection has been noted for M marinum skin infection.
M marinum infection has been reported in persons of every age group; however, it appears to be rare in the pediatric population.3
The cause is infection with M marinum.
| Cowpox Infection, Human | Sarcoidosis |
| Leishmaniasis | Sporotrichosis |
| Leprosy | |
| Nocardiosis | |
| Protothecosis, Cutaneous |
Infection with atypical mycobacteria (eg, Mycobacterium kansasii, Mycobacterium chelonae, Mycobacterium avium-intracellulare)5
Botryomycosis (Staphylococcus aureus)
Deep fungal infection (eg, with Cryptococcus neoformans, Histoplasma capsulatum, Coccidioides immitis, or Blastomyces dermatitis)
Dematiaceous fungi (chromomycosis or phaeohyphomycosis)
Infection with Francisella tularensis
Rheumatoid arthritis6
Erythema elevatum diutinum
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. Therapy must be taken regularly and continued for a sufficient period.
Found to be effective as monotherapy and is successful when given in combination with another antimicrobial. Inhibits DNA-dependent bacterial RNA but not mammalian RNA polymerase. Cross-resistance may occur. Treat for 6-9 mo or until 6 mo have elapsed from conversion to negative results from sputum culture.
600 mg PO qd
10-20 mg/kg PO/IV; not to exceed 600 mg/d
Induces microsomal enzymes, which may decrease effects of acetaminophen, oral anticoagulants, barbiturates, benzodiazepines, beta-blockers, chloramphenicol, oral contraceptives, corticosteroids, mexiletine, cyclosporine, digitoxin, disopyramide, estrogens, hydantoins, methadone, clofibrate, quinidine, dapsone, tazobactam, sulfonylureas, theophyllines, tocainide, and digoxin; blood pressure may increase with coadministration of enalapril; coadministration with isoniazid may result in higher rate of hepatotoxicity than with either agent alone (discontinue one or both agents if alterations in LFTs occur)
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Has produced liver dysfunction; urine and other secretions turn reddish; obtain CBC counts and baseline clinical chemistries prior to and throughout therapy; in liver disease, weigh benefits against risk of further liver damage; interruption of therapy and high-dose intermittent therapy are associated with thrombocytopenia that is reversible if therapy is discontinued as soon as purpura occurs; if treatment is continued or resumed after appearance of purpura, cerebral hemorrhage or death may occur
Only effective when combined with another antimicrobial agent, preferably rifampin. Diffuses into actively growing mycobacterial cells (eg, tubercle bacilli). Impairs cell metabolism by inhibiting synthesis of one or more metabolites, which, in turn, causes cell death. No cross-resistance demonstrated. Mycobacterial resistance is common with previous therapy.
25 mg/kg/d PO; not to exceed 2500 mg/d
<13 years: Not recommended
>13 years: Administer as in adults
Aluminum salts may delay and reduce absorption (give several hours before or after ethambutol dose)
Documented hypersensitivity; optic neuritis (unless clinically indicated)
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Reduce dose in impaired renal function; may have adverse visual effects, which may be reversible if promptly discontinued (physical examination should include ophthalmoscopy, finger perimetry, and color discrimination testing); elevated serum uric acid levels occur; precipitation of acute gout has been reported
Effective monotherapy; however, strains of M marinum resistant to doxycycline but sensitive to minocycline have been reported. Also treats infections caused by susceptible gram-negative and gram-positive organisms, in addition to infections caused by susceptible Chlamydia, Rickettsia, and Mycoplasma species.
100 mg PO bid
<8 years: Not recommended
>8 years: 4 mg/kg PO initially, followed with 2 mg/kg q12h
Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; tetracyclines can increase hypoprothrombinemic effects of anticoagulants
Documented hypersensitivity; severe hepatic dysfunction
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Photosensitivity may occur with doxycycline but is unusual with minocycline; reduce dose in renal impairment; tetracycline use during tooth development (last half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines; hepatitis or lupuslike syndromes may occur.
Several case reports have shown effectiveness of this drug. Reports indicate that it can help eradicate organisms unresponsive to either antituberculars or tetracyclines. Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid.
160 mg TMP/800 mg SMZ PO q12h for 10-14 d
<2 months: Not recommended
>2 months: 15-20 mg TMP/kg/d PO in 3-4 divided doses for 14 d
May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases incidence of thrombocytopenia purpura in elderly patients; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine
Documented hypersensitivity; megaloblastic anemia due to folate deficiency
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in pregnancy or breastfeeding; discontinue at first appearance of rash or sign of adverse reaction; obtain CBC counts frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged intravenous infusions or high doses may cause bone marrow depression (if signs occur, give 5-15 mg/d leucovorin); caution in folate deficiency (eg, long-term alcoholism, elderly patients, anticonvulsant therapy, malabsorption syndrome); hemolysis may occur in individuals with G-6-PD deficiency; patients with AIDS may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); give fluids to prevent crystalluria and stone formation
Cases of organisms resistant to conventional antitubercular therapy have responded to clarithromycin but not erythromycin. Use of azithromycin has not been reported. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Has bactericidal activity against atypical Mycobacterium species (eg, M marinum).
500 mg PO bid
15 mg/kg PO divided bid
Toxicity increases with coadministration of fluconazole or pimozide; effects decrease and adverse GI effects may increase with coadministration of rifabutin or rifampin; may increase toxicity of anticoagulants, cyclosporine, tacrolimus, digoxin, omeprazole, carbamazepine, ergot alkaloids, triazolam, or HMG CoA-reductase inhibitors; serious cardiac arrhythmias may occur with coadministration of cisapride; plasma levels of certain benzodiazepines may increase, prolonging CNS depression; arrhythmias and increase in QTc intervals occur with disopyramide; coadministration with omeprazole may increase plasma levels of both agents
Documented hypersensitivity; coadministration of pimozide or cisapride
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Coadministration with ranitidine or bismuth citrate not recommended with CrCl <25 mL/min; give half dose or increase dosing interval if CrCl <30 mL/min; diarrhea may be sign of pseudomembranous colitis; superinfections may occur with prolonged or repeated antibiotic therapies
Fluoroquinolones are effective alone or in combination with other medications to eradicate M marinum. Inhibits bacterial DNA synthesis and, consequently, growth.
500 mg PO bid
<18 years: Not recommended
>18 years: Administer as in adults
Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; reduces therapeutic effects of phenytoin; probenecid may increase serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Severe hypersensitivity reactions characterized by rash, fever, eosinophilia, jaundice, and hepatic necrosis with fatal outcome rarely occur; tendon ruptures requiring surgical repair or prolonged disability have been reported; crystalluria rarely occurs because human urine is usually acidic; alkalinity of urine should be avoided; may cause nervousness, agitation, insomnia, anxiety, nightmares, or paranoia; moderate-to-severe phototoxicity manifested as an exaggerated sunburn reaction can occur if directly exposed to sunlight; fatal reactions may occur when coadministered with theophylline
For treatment of tuberculosis and some atypical mycobacterial infections in combination with rifampin and other antituberculosis agents.
500-1000 mg PO qd or divided bid
<18 years: Not recommended
>18 years: Administer as in adults
Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; reduces therapeutic effects of phenytoin; probenecid may increase serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy
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mycobacterial skin infection, fish tank granuloma, tropical fish tank granuloma, M marinum, Mycobacterium, Mycobacterium marinum, mycobacteria other than tuberculosis, MOTT, nontuberculous mycobacteria, mycobacteria, acid-fast mycobacteria, saltwater infection, freshwater infection, marine infection, marine bacteria, water-borne bacteria, water-borne bacterial infection
Joslyn S Kirby, MD, Assistant Professor, Department of Dermatology, Milton S Hershey Penn State Medical Center
Joslyn S Kirby, MD is a member of the following medical societies: American Academy of Dermatology, International Society for Cutaneous Lymphomas, Pennsylvania Academy of Dermatology, and Women's Dermatologic Society
Disclosure: Nothing to disclose.
Ellen J Kim, MD, Assistant Professor, Department of Dermatology, University of Pennsylvania School of Medicine, Hospital of the University of Pennsylvania
Ellen J Kim, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, Dermatology Foundation, Medical Dermatology Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.
Saeed Jaffer, MD, MS, Assistant Clinical Professor, University of California at Los Angeles School of Medicine, Consulting Staff, Boston Dermatology
Saeed Jaffer, MD, MS is a member of the following medical societies: American Academy of Dermatology and American Society for MOHS Surgery
Disclosure: Nothing to disclose.
Terry L Barrett, MD, Clinical Professor of Dermatology and Pathology, University of Texas Southwestern School of Medicine; Director, ProPath Dermatopathology, Dallas, Texas
Terry L Barrett, MD is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, American Medical Association, American Society of Dermatopathology, College of American Pathologists, and United States and Canadian Academy of Pathology
Disclosure: Nothing to disclose.
Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.
Lester F Libow, MD, Dermatopathologist, South Texas Dermatopathology Laboratory
Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Texas Medical Association
Disclosure: Nothing to disclose.
Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.
Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.
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