2011 07 Microbiology-Mycobacterium skin infection

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I.MYCOBACTERIUM LEPRAEA. HistoryDiscovered in 1873 by G.A. Hansen

Causes Hansens Disease or Leprosy(no effective therapy until 1940)

In Spain: Lepers- Legally dead, a socialstigma (marker for isolation)

B.Diagnostic Features An obligate Intracellular parasites that

needs a host to replicatePrefers to attack Macrophages and

Schwann cells

Acid-fast staining straight or slightlycurved rods, arranged singly, in parallel

bundles or globular masses

Red Stain (seen in smears) Gram Variable - more gram(+) than

gram(-)

not really useful for identification Regularly found in scrapings from the

skin or mucous membrane (nasal

septum- has lower temp.

Bacilli from ground tissue nasalscrapings:

1. Inoculated into footpads of mice-->development of local

granulomatous lesions with limited

bacterial multiplication

2. Inoculated into armadillosdevelopment of extensive

lepromatous/leprosy

Take note: nasal scrapings contain a very

high number of the organisms because they

prefer to stay in the cooler part of the body,

and the nasal septum temp is lower than

any other part of the body.

Bacilli are often found withinendothelial cells of blood vessels or in

mononuclear cells

Humans and Nine-banded armadillosare the only known natural hosts

Has mycolic acid which gives it a thinwaxy coating

Mycolic acid- large fatty acid;dense, large lipid outer capsule

outside the cell wall (phenolic

glycolipid 1 or PGL-1) which has

served as the antigen for serologic

test for leprosy

CANNOT be grown in cell-free media ortissue culture

Grows best at below 37C in humansand mice (predilection for cooler areas

of body)

Grows luxuriously in cold bloodedarmadillos

Gram(+) bacillus under Ziehl-Neelsenstaining method

Fig.1: A tissue section: Red- mycobacterium

acid-fast

C. Epidemiology-estimated 6 million with leprosy (3 million

untreated)

- Endemic: Asia (greatest number cases),

Africa, Latin America, and Pacific

- Associated with: poverty, rural residence,armadillo contact (N. America)

- Transmission is due to overcrowding and

poor hygiene

- Modes of Transmission:

1. Majority - nasal droplet infection

2. Skin-to-skin contact - not the

general route because organisms are

not found histologically in the

epidermis nor the dermis

3. Contact with lepromatous leprosy

patients (shedding of organisms innasal secretions or ulcer exudates)

Outline:

I. Mycobacterium Lepraea. Historyb. Diagnostic Featuresc. Epidemiologyd. Clinical Manifestatione. Typesf. Lepromin testg. Laboratory Diagnosish. Treatmenti. Prevention and Control

II. Mycobacterium Marinuma. Diagnostic Featuresb. Clinical Manifestationsc. Clinical Diagnosisd. Treatment

III. Mycobacterium Ulceransa. Diagnostic Featuresb. Epidemiologyc. Clinical Manifestationsd. Treatment

Subject: MicrobiologyTopic: Mycobacterial Skin InfectionsLecturer: Dr. Teresa Barzaga MDDate of Lecture: 07-20-2011

Transcriptionist: Bunny Fril

Editor: in Chief

Pages: 5SY

2011-2012


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4. Insect vectorsbed bugs and

mosquitoes in areas of leprosaria

community harbor M. Leprae

5. Transmitted by soil:

a.) M. Leprae specific PGL-1 has

been found in soil

b.)Leprosy is primarily a rural and

not an urban disease

c.) Direct dermal inoculation such

as in tattoo parlors has been

associated with disease transmission

Incubation period: minimum of 2-3

years; can be as long as 40 years

Long Incubation period: M. Leprae multiplies very slowly

(doubling every 14 days in mice)

The number of bacilli harbored bylepromatous patient on initialdiagnosis if far greater than that

of any human bacterial disease

D. Clinical ManifestationsLargely confined to the skin, Upper

respiratory tract, testes, and

peripheral nerves

Most serous sequelae: small nervefibers are functionally impaired (loss

og touch, pain, hot and cold

sensation- result of topism forperipheral nerves)

E. Major Types

Fig.2: Tuberculoid leprosy

Fig.3 Tuberculoid type of leprosy

Fig. 4 Leonine Facies- Lepromatous Leprosy

Fig. 5 Leonine Fascie- lepromatous type of

leprosy

F.Lepromin Test- Intradermal skin test using heat killed

human or armadillo derived M.

Leprae

- Not diagnostic- Test lacks specificity

CATEGORY TUBERCULOID LEPROMATOUS

Course

Non-

progressive;

benign

Progressive;

malignant

Skin lesions Macular Nodular

Acid Fast

Organisms(AFB) in skin

Few Abundant

Nerve

Involvement

Severe,

sudden,

asymmetric

Slow symmetric

Lepromin

skin testPositive Negative

Cell-

mediated

immunity

Intact Deficient

Skin

infiltrates

Helper T-cellSuppressor T-

Cells


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- Can be induced in normal healthyindividuals by vaccination with BCG

G. Laboratory Diagnosis1.Demonstration of AFB (acid-fast

bacilli) in smears of:

a. Nasal scrapingsb. Skin lesionsc. Ear lobes- lower temp;

organisms can be taken

from here

2.Tissue sections3.Biopsy of Skin or thickened nerve4.Culture in footpads of mice

Fig.6 Section of the skin, showing abundant

organisms (acid-fast bacilli)

Fig. 7 Section of the Skin, Acid fast bacilli,

underneath the dermis

H. Treatment- Sulfones- Rifampicin- Clofazimine*take note: treatment should be

continued until skin smears become

negative

I. Prevention and Control1.Identification and treatment of case2.Children of presumably contagious

parents has rendered them

noninfectious

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II. MYCOBACTERIUM MARINUMA. Diagnostic Features

- From salt water dead fish- Can cause tuberculosis

- Slow growing- Grow optimally at low temp. (32C)- Shares other antigens with other

mycobacteria

- Inhibits water and marine organism- Incubation period: 2-3 weeks- Infection follows:

o After minor trauma ininfected swimming pools,

aquariums or natural bodies

of water

o Trauma from fish spines ornips by crustaceans

*Infection is common among fish

handlers and swimmers

- Disease almost always confined tosuperficial cooler body tissues, most

often on the extremities- Typical presentation: Single

inflammatory nodule that is seen in

the elbows, knees or on the feet of

swimmers, or hands of fish

handlers begin as small

papulesenlarges acquire a blue

purple hue suppuration progress

to ulceration

Take note: lesions are called swimming

pool granulomas or fish-tank

granulomas

B. Diagnosis1.Culture of skin lesions (definitive

diagnosis)

Organisms grow best at 30C-35C

2.Histologic examPresence of granuloma + clinical

history (suggestive of the

diagnosis)

*most strains are resistant to IMH,

para-amino-salicylic acid and

streptomycin

C. Treatment*most strains are resistant to INH, PAS

and SM

1. good results with Rifampicin and

EMB

2. Tetracyclines

3. TMP- SMX

Fig. 8


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Fig. 9 lesions on the hand

Lesion seen in the arm with hemorrhage and

ulceration

Supposed to be red acid-fast bacterium (but the

picture given was black and white)

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III.MYOBACTERIUM ULCERANSA. Diagnostic Features

- Slow growing, belongs to a large groupof environmental Mycobacteria

-

Inhabits water where it can colonizeaquatic plants, herbivorous animals

and aquatic insects

- Endemic in countries with tropicalrainforest

- Causes chronic, painless, cutaneousulcers (Buruli ulcers- Uganda;

Bairnsdale ulcers- Australia)

- Prefer cooler temperatures (30C-35C) seen at the extensors of the

body (hands and feet)

- Ulcers: seen in extensor surface ofextremities

- Prevalent in Australia (median agegroup 50-66) and Africa (peak age 5-

15)

Take note: (worldwide infection)

*1st

most common: mycobacterium tuberculosis

*2nd

most common: mycobacterium leprae

*3rd most common: mycobacterium ulcerans

B. Transmission- not fully understood- linked in contaminated water

1. abraded skin2. probably via skin trauma

(contaminated with water, soil or

vegetation)

3. insects play an important role- ONLY mycobacterium to cause disease

by the production of TOXINS- Toxins produced are called

Mycolactum - lipid molecule, it

diffuses at the side of infection and at

the surrounding skin to kill the

surrounding cells and suppresses the

immune response of the patient

- lesionbegins as a nodule ulceratesover 4-6 weeks

Centers of ulcer necrotic withoutceasation

Organisms are located at theperiphery, adjacent to normaltissue

C. TreatmentSuccess has been reported with:

1.Local heat, excision and skin grafting2.Combination of either INH-

Streptomycin or

diaminodiphenylsulfone plus

oxytetracycline

3.Combination of SMX, RMP andminocycline

Note the location of the lesion. Mycobacterium

likes to stay at cooler temp part of the body


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Caused by Mycobacterium ulcerans

_______________fin___________

Luke, I am your Father

-Darth

Vader

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---------------------------------

From BUNNY FRIL:***HELLO Everyone! Hello Friendsand Fiends! (wag ng isa-isahin,saying ung ink!) STUDY WELL!!!And WE ROCK!!!***first tranx na ginawa namin,kaya pagpasensyahan niyo na ha.

***this tranx were based from

the powerpoint, recording,

previous tranx and some infos

were pulled out from nursery

books.

*** Lizette! Ikaw na ang may

malaking tooooot IKAW NA ! IKAW

NA ANG MAY LAHAT!!!

From THE CHIEF:

***DISCLAIMER: kapag may mali,

please inform the batch agad

(thru FB or whatever means).

Thank you. AND walang

sisihan!!!hahaha hope this tranx

will suffice.

***ung pictures, baka malabokapag xinerox na, nasa FB naman

ung powerpoint slides, so check


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2011 07 Microbiology-Mycobacterium skin infection

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