eMedicine Specialties > Dermatology > Bacterial Infections

Malakoplakia: Treatment & Medication

Author: Raphael J Kiel, MD, Associate Professor of Medicine, Wayne State University School of Medicine; Consulting Staff, Infectious Diseases Division, William Beaumont Hospital
Contributor Information and Disclosures

Updated: Oct 21, 2008

Treatment

Medical Care

  • Therapy with antibiotics that concentrate in macrophages (eg, quinolone, trimethoprim-sulfamethoxazole) is associated with a high cure rate. Antibiotic therapy directed against E coli in combination with surgery provides the best chance of cure.
  • Bethanechol, a choline agonist, has been used in combination with antibiotics and surgery. Bethanechol may correct the decreased cGMP levels that are believed to interfere with complete bacterial killing.
  • Ascorbic acid has been used to increase the cGMP and cyclic adenosine monophosphate (cAMP) levels in monocytes, which may represent an effective strategy for therapy. An insufficient number of patients have been treated with ascorbic acid to determine its overall effect.
  • Discontinuation of immunosuppressive drug therapy is usually needed to effectively treat malakoplakia.

Surgical Care

  • Excision of skin lesions and drainage of abscesses are fundamental to diagnosis and treatment.
  • Surgery combined with antibiotic therapy should be directed against E coli or other organisms recovered on culture.

Consultations

  • Dermatologist
  • Infectious disease specialist

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Antibiotics

Antimicrobials directed against gram-negative bacteria, especially E coli, are used to treat patients with malakoplakia. In addition, antibiotics that concentrate in macrophages are used. Quinolone antibiotics (eg, ciprofloxacin) and sulfonamides (eg, trimethoprim-sulfamethoxazole) are indicated. Bethanechol and ascorbic acid have also been used in the treatment of patients with malakoplakia.


Ciprofloxacin (Cipro)

Fluoroquinolone that has activity against Pseudomonas and Streptococcus species, MRSA, Staphylococcus epidermidis, and most gram-negative organisms but has no activity against anaerobes. Inhibits bacterial DNA synthesis and, consequently, growth. Continue treatment for at least 2 d (7-14 d typical) after signs and symptoms have disappeared.

Adult

250-500 mg PO bid for 7-14 d

Pediatric

<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)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

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


Trimethoprim and sulfamethoxazole (Bactrim, Bactrim DS, Septra, Septra DS)

Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. Antibacterial activity of TMP-SMZ includes common urinary tract pathogens except P aeruginosa.

Adult

160 mg TMP/800 mg SMZ PO q12h for 10-14 d

Pediatric

<2 months: Do not administer
>2 months: 10-20 mg TMP/kg/d PO/IV divided tid/qid 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 with 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

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Discontinue at first appearance of skin 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 IV infusions or high doses may cause bone marrow depression (if signs occur, administer 5-15 mg/d leucovorin); caution in folate deficiency (eg, patients with chronic alcoholism, elderly patients, patients receiving anticonvulsant therapy, patients with malabsorption syndrome); hemolysis may occur in patients 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); administer fluids to prevent crystalluria and stone formation

Cholinergic agents

These agents increase the contractility of the bladder.


Bethanechol hydrochloride (Duvoid, Myotonachol, Urabeth, Urecholine)

Used for selective stimulation of the bladder to produce contractions to initiate micturition and to empty the bladder. Found to be most useful in patients who have bladder hypocontractility, provided they have functional and coordinated sphincters. Rarely used because of difficulty in timing the effect and because of gastrointestinal tract stimulation.

Adult

10-50 mg PO tid/qid

Pediatric

Not established

Concurrent administration with ganglion-blocking compounds may cause decrease of blood pressure to critical levels

Documented hypersensitivity; peptic ulcer disease; obstructive pulmonary disease; bradycardia; vasomotor instability; hypotension; atrioventricular conduction defects; hyperthyroidism; epilepsy; mechanically obstructed GI or GU tract

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Urinary retention secondary to possible reflux of urine into kidneys may occur

Vitamins

Vitamins with the ability to induce collagen fibril synthesis are used.


Ascorbic acid (C-Crystals, Ascorbicap, Cevi-Bid, Vita-C)

For collagen synthesis and tissue repair.

Adult

100-250 mg PO qd/bid for a minimum of 2 wk

Pediatric

100-300 mg PO in divided doses for a minimum of 2 wk

Decreases effects of warfarin and fluphenazine; increases aspirin levels

Documented hypersensitivity; pregnancy if large dose used

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Pregnancy category C when doses higher than RDA used; prolonged high doses may cause renal calculi, especially in patients with diabetes

More on Malakoplakia

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Differential Diagnoses & Workup: Malakoplakia
Treatment & Medication: Malakoplakia
Follow-up: Malakoplakia
Multimedia: Malakoplakia
References

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Further Reading

Keywords

malakoplakia, malacoplakia, soft plaque, genitourinary tract plaque, genitourinary tract nodule, GU tract nodule, GU tract plaque, cutaneous malakoplakia, cutaneous malacoplakia

Contributor Information and Disclosures

Author

Raphael J Kiel, MD, Associate Professor of Medicine, Wayne State University School of Medicine; Consulting Staff, Infectious Diseases Division, William Beaumont Hospital
Raphael J Kiel, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine and American Geriatrics Society
Disclosure: Nothing to disclose.

Medical Editor

Peter Fritsch, MD, Chair, Department of Dermatology and Venereology, University of Innsbruck, Austria
Peter Fritsch, MD is a member of the following medical societies: American Dermatological Association, International Society of Pediatric Dermatology, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: 3M Pharmaceutical Grant/research funds Other; Graceway Pharmaceuticals Grant/research funds Other

Managing Editor

Jeffrey J Miller, MD, Associate Professor, Department of Dermatology, Penn State University, Milton S Hershey Medical Center
Disclosure: Nothing to disclose.

CME Editor

Glen H Crawford, MD, Assistant Clinical Professor, Department of Dermatology, University of Pennsylvania School of Medicine; Chief, Division of Dermatology, The Pennsylvania Hospital
Glen H Crawford, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Phi Beta Kappa, and Society of USAF Flight Surgeons
Disclosure: Nothing to disclose.

Chief Editor

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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