DEPARTMENT OF PATHOLOGY
The Johns Hopkins Medical Institutions

Vol. 21, No. 8
THE JOHNS HOPKINS MICROBIOLOGY NEWSLETTER
Tuesday, March 5, 2002

  1. Provided by Karen Fujii, Division of Outbreak Investigation, Maryland Department of Health and Mental Hygiene.

    2. 12 outbreaks were reported to DHMH during MMWR Week 9 (February 24 - March 2):
4 outbreaks of respiratory illnesses
* 2 outbreaks of INFLUENZA-LIKE ILLNESS (1 at a nursing home in Montgomery Co.; 1 at a nursing home in Baltimore Co.)
* 1 outbreak of INFLUENZA-LIKE ILLNESS/PNEUMONIA at a nursing home in Wicomico Co.
* 1 outbreak of RESPIRATORY SYNCYTIAL VIRUS at a hospital in Howard Co.
4 outbreaks of GE-type illnesses
* 3 GASTROENTERITIS outbreaks (2 in Montgomery Co. [1 at an assisted living center; 1 at a nursing home]; 1 at a nursing home in Howard Co.)
* 1 FOODBORNE GASTROENTERITIS outbreak associated with a grocery store in Montgomery Co.
* 1 Pseudomonas cluster identified at a hospital in Baltimore City
* 1 FOLLICULITIS outbreak at an athletic club in Harford Co.
* 1 CONJUNCTIVITIS outbreak at a nursing home in St. Mary's Co.
* 1 RASH ILLNESS outbreak at a school in Wicomico Co.   B. The Johns Hopkins Hospital, Department of Pathology, Information provided by M. Ali Ansari-Lari, MD, Ph. D.
Case presentation: An otherwise healthy 2 year-old Caucasian male presented to the Pediatric Clinic at The Johns Hopkins Hospital with six-week history of right submandibular swelling, which was gradually becoming larger. Two separate fine needle aspiration of the mass were performed in an outside hospital, one showing necrotic material raising the concern for tumor, and the other one showing acid fast bacilli. He has been treated with antibiotics (not specified) without any change. He has not had any systemic symptoms such as fever, cough, weight loss or sweats. He has not been exposed to any cats. Chest x-ray and PPD skin test have not been done. His physical examination was remarkable for a 2.5 X 1.5 cm fluctuant, nontender mass along the inferior boarder of the right mandible, posterior to the submandibular gland. The skin overlying the mass showed central erythema with thinning. He underwent curettage and debridement of the mass. Histologic examination revealed necrotizing granulomatous inflammation with mycobacterial organisms identified on an auramine-rhodamine immunofluorescent stain. The culture grew Mycobacterium avium intracellulare complex (MAC).
Mycobacterial lymphadenitis

Organism identification:

MAC has traditionally consisted of 28 serotypes of two distinct species, M. avium and M. intracellulare (1). The classic strains of M. avium were originally included in the group III nonphotochromogens in the Runyon classification. However, strains recovered from patients with AIDS may have a distinct yellow pigmentation (2). On microscopic examination using Ziehl-Neelsen, Kinyoun, or auramine-rhodamine staining with fluorescent microscopy, the MAC organisms may appear as short coccobacilli or long, thin bacilli. Except for production of heat-stable catalase and ability to grow on T2H, other biochemical reactions for mycobacterial speciation are negative. DNA probes (acridinium ester-labeled AccuProbes) complementary to species-specific sequences of rRNA are available for identification of MAC. Additionally, analysis of mycobacterial fatty acids by chromatography can be performed. Clinical presentation and epidemiology: MAC is ubiquitous in nature and has been isolated from soil, water, plants, house dust and other environmental sources. In healthy, immunocompetent individuals, MAC has been considered to have a low pathogenicity and rarely cause disease. MAC can colonize healthy persons, although the rate of colonization in immunocompetent healthy children is unknown. The portal of entry appears to be via the lymphatic vessels that drain the mouth and the pharynx. MAC has been isolated from gastric aspirates of two immunocompetent children with cervical lymphadenitis by polymerase chain reaction (3). Other potential portals of entries include the gingivae and oropharyngeal mucosa (4). The prevalence of mycobacterial lymphadenitis is not known since a proportion of cases may remain subclinical, accounting for some of the positive PPD skin tests during routine surveillance (4).

In one large prospective study conducted from 1958 to 1990, the medical records of 105 children with mycobacterial lymphadenitis were reviewed (4). The age range was from 9.5 months to 12 years with median age of 2.92 years. There was a slight female predominance (1.3: 1 female to male). While the incubation period from infection to clinically apparent lymphadenopathy was unknown, the onset of disease occurred twice as often in the winter and spring than the summer and fall seasons. In nearly all cases, patients were brought to the clinical attention because of unilateral cervical or facial swelling, predominantly in the submandibular area. Bilateral cervical lymphadenopathy was noted in about 5% of the cases. There were no reported cases of disseminated disease. In the majority of cases, children were afebrile and appeared healthy without any historical or physical evidence of immune dysfunction, abnormal blood counts or abnormal chest x-ray. The most common histologic finding was caseating granulomatous inflammation. In almost all of the cases, the PPD skin test was positive (6-15 mm induration), with long-lasting reactivity. From 1958 to 1978, the predominant isolated species was M. scrofulaceum. However, after 1978, the most common isolated species was MAC. The reason for the abrupt change in the etiologic agents is not known. Although rare, other reported mycobacterial species resulting in cervical lymphadenitis include M. kansasii, M. fortuitum, M. haemophilum, M. interjectum, M. szulgai, M. xenopi, and M. malmoense. In areas where tuberculosis is endemic, M. tuberculosis is the most common cause of cervical adenitis.

The differential diagnosis of non-mycobacterial cervical lymphadenopathy includes pyogenic adenitis, cat scratch disease, mumps, infectious mononucleosis, sialadenitis, congenital cysts, and malignancy.

 Treatment: The treatment of choice is early surgical resection (4). Biopsy and incision and drainage should be avoided due to potential complication of fistula formation. Other complications include recurrence because of incomplete excision, and facial nerve damage. Most strains of MAC are resistant to commonly used antituberculous drugs. Combinations of clarithromycin and ethambutol or clarithromycin and rifabutin have been reported to be effective against nontuberculous mycobacterial lymphadenitis (5,6). References:
    1. Murry, PR, Baron, EJ, Pfaller, MA, Tenover, FC, Yolken, RH. Manual of clinical microbiology (7th edition). 1999. ASM Press, Washington, DC.
    2. Koneman et. al. Color Atlas and Textbook of Diagnostic Microbiology, 5th Edition, Lippincott-Raven, Philadelphia, 1997.
    3. Haas WH, Amthor B, Engelmann G, Rimek D, Bremer HJ. Preoperative diagnosis of Mycobacterium avium lymphadenitis in two immunocompetent children by polymerase chain reaction of gastric aspirates.

      4. Pediatr Infect Dis J. 1998 17:1016-20.
    4. Wolinsky E. Mycobacterial lymphadenitis in children: a prospective study of 105 nontuberculous cases with long-term follow-up. Clin Infect Dis. 1995 20:954-63.
    5. Green PA, von Reyn CF, Smith RP Jr. Mycobacterium avium complex parotid lymphadenitis: successful therapy with clarithromycin and ethambutol. Pediatr Infect Dis J. 1993 ;12:615-7.
    6. Berger C, Pfyffer GE, Nadal D. Treatment of nontuberculous mycobacterial lymphadenitis with clarithromycin plus rifabutin. J Pediatr. 1996;128:383-6.
 

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