Atypical Mycobacteria

Question 1

General features of atypical mycobacteria?

Answer 1

– Common in soil, water, dust, food stuffs

– Frequent contaminants of clinical specimen

– May colonize body surfaces for prolonged times without causing disease

– Differentiation between contamination, colonization, and disease is difficult

Question 2

What are the atypicals in Photochromogenes (Runyon Group I)

Answer 2

• M. kansasii • M. marinum • M. simia

Question 3

Atypical mycobacteria in Scotochromogens (Runyon Group II)?

Answer 3

• M. scrofulaceum • M. szulgai • M. gordonae • M. flavescens

Question 4

atypical mycobacteria in Nonchromogens (Runyon Group III)?

Answer 4

• M. avium-intracellulare • M. xenopi • M. ulcerans • M. gastri • M. terrae • M. triviale

Question 5

Atypical mycobacteria that are Rapid Growers (Runyon Group IV)?

Answer 5

• M. fortuitum • M. chelonae • M. smegmatis

Question 6

Guidelines to implication in disease for atypicals?

Answer 6

• Patients illness consistent with a non-atypical mycobacterial syndrome
• Other causes of disorder (fungal, TB) excluded
• Species of mycobacterium crucial
• Site of origin positive culture crucial – Sterile sites always significant
• Quantity of growth of the culture important
• Repeated isolation of the organism from body secretion

Question 7

General features of M.Kansasii?

Answer 7

M. Kansasii – General

– Water is a natural reservoir

– Southwest, Midwest

– Men > Women –5 th decade

– High risk • Pneumoconiosis • COPD • Immunodeficient

Question 8

Clinical disease of M. Kansasii?

Answer 8

–Pulmonary infection • Mild chronic symptoms • Physical exam minimal • Chest x-ray (may be similar to TB) • Sputums – Repeatedly positive without other cause – May coexist with TB

– Lymphadenitis

– Syndrome resembling sporotrichosis

– Cellulitis

– Osteomyelitis

– Hypersensitivity syndrome (E. nodosum)

– Dissemination • Immunocompromised • Pancytopenic

Question 9

Therapy for M.Kansasii?

Answer 9

• Therapy – INH, RMP, EMB

Question 10

Epidimiology and risk factors for Mycobacterium avium complex?

Answer 10

– Isolated sources • Soil, natural, municipal water, food, host dust, domestic, wild animals • Inhalation of aerosols • No person-to-person spread

– Risk Factors • Chronic lung disease • Gastrectomy • T-cell deficiency (<100) • Lung disease seen in “normal people”

Question 11

Symptoms of MAC in AIDS patients?

Answer 11

– Gastrointestinal • Nausea, vomiting, diarrhea, abdominal pain, colitis, ileal and duodenal involvement

– Hematologic • Anemia, neutropenia

– Systemic • Fever, chills, night sweats, wasting syndrome, liver involvement (alkaline phosphatase)

– Pulmonary • Unusual site

Question 12

Symptoms of MAC in non-AIDS patients?

Answer 12

Question 13

Diagnosis of MAC?

Answer 13

– Sputums • Normal colonization • Pathogen if underlying cavities, infiltrates

– Blood Cultures

– Lymph nodes, bone marrow, liver biopsies

– Methods • AFB smear • Cultures • DNA probe • PCR

Question 14

Therapy for MAC?

Answer 14

– Very resistant

– Requires multiple drugs

– Disseminated disease • Clarithromycin or Azithromycin • Ethambutol • Rifabutin

– Prophylaxis • Clarithromycin • Azithromycin

Question 15

M.Marinum Location? infection?

Answer 15

– Trauma to skin • Swimming pools, aquariums, natural bodies of water • Fish spines, nips of crustaceans

– Local Infection • Papule ulcer • Sporotrichoid type spread

Question 16

Therapy for M.Marinum?

Answer 16

Therapy • Rif, EMP • Tetracyclines • Trimethoprim - sulfamethoxazole

Question 17

M. Scrofulaceum location? clinical findings?

Answer 17

– Frequently contaminates specimens, reagents, standing water

– Colonize respiratory secretions of well indiviulas

– Clinical • Lymphadenitis, submandibular area • Children age 1-3 years • Enlarge slowly over weeks • May rupture with draining sinus

Question 18

What is the differnential and therapy for M. Scrofulaceum?

Answer 18

– Differential • M. Tuberculosis • PPD (-)

– Therapy • Surgical removal

Question 19

Rapid growing mycobacterium, are which ones? human infections how? require how much time to grow?

Answer 19

• Requires 2 to 30 days for growth
• Isolated from tap water, municipal water, moist areas in hospitals, contaminated biologicals, aquariums, domestic animals
• Human infections acquired – Trauma, infection, surgery
• Species – M. Chelonei – M. Abscessus – M. Fortuitum

Question 20

Clinical syndromes of the rapid growing mycobacterium?

Answer 20

– Infections of skin and soft tissue

– Cardiac surgery, augmentation mammoplasty, peritoneal dialysis, arthroplasty

– Bronchopulmonary infections • May colonize respiratory secretions without disease

– Other diseases • Lymphadenitis, keratitis, osteomyelitis, meningitis – Disseminated Disease • Majority immunodeficient

Question 21

What are the rave species and what do they cause clinically?

Answer 21

• M. Szulgai – Pulmonary disease similar to M. tuberculosis
• M. Xenopi – Pulmonary disease – Human tonsils (colonizer)
• M. Malmoense – Pulmonary disease – Lymphadenitis – Disseminate
• Post-Surgical Infections – Augmentation mammoplasty – Median sternotomy – Prosthetic joint – Percutaneous catheter – Pacemaker insertion – Lipoma excision – Facial plastic surgery – Cervical laminectomy – Saphenous vein removal – Knee repair
• Primary Cutaneous Infections – With or without osteomyelitis
• Pulmonary Infections
• Disseminated Disease
• Miscellaneous – Keratitis and corneal ulceration – Prosthetic valve endocarditis – Cervical lymphadenitis – Meningitis – Hepatitis – Synovitis – Epidural abscess

Question 22

How do you treat the rapid growing mycobacterium?

Answer 22

– M. Chelonae • Clarithromycin-sensitive • Amikacin, doxycycline, imipenem variable

– M. Fortuitum • Amikacin, Cefoxitin, Ciprofloxacin, Ofloxacin, Sulfonamide

– M. Abscessus • Amikacin, Cefoxitin

Question 23

What do the rave species M.Haemophilum and M.Ulcerans cause?

Answer 23

• M. Haemophilum – Skin and subcutaneous lesions (immunocompromised)
• M. Ulcerans – Chronic, painless cutaneous (Buruli) ulcers – Extensor surfaces of extremities

Question 24

Explain the general features of Mycobacterium Leprae?

Answer 24

– Acid fast, slightly curved bacillus

– Metachromatic granule near pole or center

– Contains mycolic acids (as other mycobacteria)

– Large amounts specific phenolic glycolipid

– Loss of acid fastness by pyridine extraction

– Characteristic slow growth curve in footpads of mice

– Ability to oxidize dihydrooxyphenylalanine (DOPA)

– Tendency to infect peripheral nerves of humans

Question 25

Epidemiology of Mycobacterium Leprae?

Answer 25

– Skin not major mode of spread

– Nasal discharge high amount of organisms (1x108/ml)

– Respiratory tract

– Breast milk

– Biting insects may transmit

– Lepromatous • 20% incidence in India • 30-50% incidence in Japan, China, Korea

– Tuberculoid • Up to 90% in Africa

Question 26

Explain the pathology of both the tuberculoid and Lepromatous forms of Mycobacterium Leprae?

Answer 26

– Tuberculoid • Histology similar to sarcoid granulomas • Nerve bundles that are grossly swollen and infiltrated with mononuclear cells • Acid-fast bacilli few to absent • Able to manifest delayed-type hypersensitivity to skin tests

– Lepromatous • Predominant cell is macrophage • Langhan type giant cells, lymphocytes are few • Granulomas not developed • Numerous acid fast bacilli • Profoundly anergic

Question 27

Clinical spectrum of M.Leprae?

Answer 27

– Full tuberculoid • Large erythematous plaques with sharply demarcated raised outer edges • Area is anesthetic • May have damaged few peripheral nerves

– Borderline tuberculoid – Borderline Borderline • Skin manifestations more numerous • Raised satellite lesions present • Anesthesia less marked

– Full lepromatous • Extensive bilateral, symmetrical erythematous macules, papules or nodules • Advanced skin thickening of face, nose, ears (classic leonine facies) • Destruction nasal-maxillary structures • Nerve involvement patchy less severe