hansen disease medical microbiology presentation by ruth naomi manuel

HANSEN’S DISEASE

DIPLOMA IN MEDICAL

SCIENCE

SCHOOL OF ALLIED

SCIENCE

WINDFIELD INTERNATIONAL

COLLEGE

HANSEN’S DISEASE

RUTH NAOMI MANUEL

SARAVANAN A/L SURESH

SRIRENUKAA A/P MARIMUTHU

INTRODUCTION

Also known as leprosy

Chronic infectionCaused by Mycobacterium Leprae & Mycobacterium

Lepromatosis

Affects skin, nerves & eyes

• Paucibacillary - 5 or less poorly pigmented numb skin patches present

• Multibacillary - More than 5 poorly pigmented numb skin patches present

Two main types of disease based on the number of bacteria present-

TYPES OF LEPROSY

1-Indeterminate leprosy-

A few hypopigmented macules

can heal spontaneously

2-Tuberculoid leprosy-

A few hypopigmented macules

some are large and some become anesthetic

(lose pain, tactile and termic sensation)

nerves become enlarged; spontaneous resolution

Borderline tuberculoid leprosy-

Lesions like tuberculoid

leprosy but smaller and

more numerous with less nerve

Enlargement nerves; this form may

persist, revert to tuberculoid

Mid-borderline leprosy-

Many reddish plaques

asymmetrically distributed, moderately anesthetic

regional adenopathy

(swollen lymph nodes)

Histoid leprosy lepromatous leprosy that

presents with clusters of histiocytes

(a type of cell involved in the inflammatory

response)

A grenz zone

(an area of collagen

separating the lesion from

normal tissue)

Lepromatous leprosy Early lesions are pale macules ;

(flat areas) that are diffuse and

symmetric

Alopecia (hair loss) ; often

patients have no eyebrows

nerve involvement

leads to anesthetic areas

& limb weakness;

progression leads to aseptic

necrosis (tissue death from lack of blood to area)

lepromas (skin nodules)

disfigurement of many areas

including the face

CAUSES• An intracellular, acid-fast bacterium• Aerobic & rod-shaped bacterium• surrounded by the waxy cell

membrane• does not form capsules, flagella, or

spores

Mycobacterium leprae &

Mycobacterium lepromatosis

• Are obligate pathogens• Are unculturable in laboratory

Due to extensive loss of genes necessary for independent

growth ;

Mycobacterium Leprae

Electron Micrograph

Acid Fast

Gram Staining

MODE OF TRANSMISSION

Person to person-leprosy spread from person to

• through infected respiratory

droplets• Through close contact with the affected person

Genetics• Parents of someone with

leprosy• Children of someone with

leprosy

The extent of exposure

Environmental conditions

• Poor hygiene condition

PATHOGENECITY (VIRULENCE FACTOR)

Iron utilization

• Help the pathogen acquire nutrients for growth• NRAMP proteins

• Allow transportation of iron into the macrophage for survival

Waxy

exterior

• Allows intake into the macrophage and into some dendritic cells in which it can survive

Macropha

ge invasion

• Prevent phagosome and lysosome fusion to avoid degradation

• Bacteria are absorbed into the phagolysosome

Schwann cell invasion

Major target of Mycobacterium leprae

To access the cells, Mycobacterium leprae gets

into the lymphatic system and the blood vessels

Mycobacterium leprae binds to the Schwann cell via laminin-binding protein

The bacteria will enter through the vascular

epithelium into the cell

Drug resistance

Allow it to continue to survive despite

antimicrobial presence

PATHOGENESIS

Mycobacterium leprae

has a difficult time

replicating outside of host cells

It is a very slowly

replicating bacteria that can take up to 13 days

Leprosy - bacterial replication inside intracellular vesicles • macrophages,

Schwann cells, & endothelial cells

CELL BINDING

Bacteria binds to receptors on the host cell surface

In neural Schwann cells, the phenolic glycolipid-1 (PGL-1) or LBP21 receptor on M. leprae binds to the α-2 side chain of laminin-2 & α-dystroglycan receptor(1)

Presence of the histone-like protein Hlp, secreted by M. leprae, enhances Schwann cell binding

Facilitates phagocytosis by the classical complement pathway

Once binding has occurred, M.

leprae is taken into the host cell by phagocytosis

and is encapsulated by

a phagosome

Survive phagosome-lysosome fusion & live long

enough to replicate

Replication will take

place

SIGNS & SYMPTOMSLeprosy symptoms generally appear three to five years after a person becomes infected with bacteria

Skin lesions that are lighter than your normal skin color; lesions have decreased sensation to touch, heat, or pain and lesions do not heal after several weeks to months

Numbness or absent sensation in the hands, arms, feet, and legs

Muscle weakness

Eye problems

Skin rash

Skin stiffness

Hypopigmented Macule Deformity

Skin Lesions

EXAMS AND TESTS

Lepromin skin test • D

istinguish lepromatous from tuberculoid leprosy, but is not used for diagnosis.

Skin lesion biopsy.

Different tests can be employed in the diagnosis of different type of

leprosy

Epidemicology Triangle of Leprosy

Agent- Mycobacterui

m leprae

Environment- Transmitted by

person to person contact

Host – Infected to

human

Lab Diagnosis

Skin lesion biopsy

CBC

PCRLiver blood

Creatinine blood

Lepromin skin

Types of Skin biopsy

Shave biopsy

Punch biopsy

Exicisional biopsy

Incisional biopsy

Shave Biopsy

least invasive method.

Your doctor uses a small blade to

remove the outermost layers

of skin.

The area removed includes all or part

of the lesion.

Do not need stitches.

At the end of the procedure, medicine is

applied to the area to stop any

bleeding.

Excisional Biopsy

usually done by

a surgeon. During the

procedure, the entire lesion is

removed.

Numbing medicine is

injected into the

area.The entire lesion is

removed, going as deep as

needed to get the

whole area.

The area is closed with

stitches. If a large area is biopsied, a skin graft or flap of

normal skin may be used to

replace the skin that was removed.

Incisional Biopsy

CBC ( Comp

lete Blood

Count )

Most commonly ordered

blood tests.

The complete

blood count is

the calculation of the cellular (formed

elements) of blood.

Determined by

special machines

that analyze

the different compone

nts of blood in less than a minute.

To measure

of the concentra

tion of white blood

cells, red blood

cells, and platelets

in the blood.

PCR (Polymerase

Chain Reaction)

PCR recombined

DNA technology

have allowed for

development of genes M.leprae

Used in biopsy

samples , blood and

tissue section

Liver

blood test.

Most

common

ly performed

blood

tests.

Can be

used to

assess

liver functions or liver injur

y.

An initial step is a

simple blood test to determine the

level of

certain liver

enzymes

(proteins) in the

blood.

But when the liver

is injured for any

reason,

these enzymes are

spilled

into the

blood

stream.

Creatinine blood test.

If the kidney become impaired

, the creatinine level rise due to

poor clearance of creatinine by the

kidney.

Found to be a fairly reliable indicator of

kidney function.

Elevated creatinine level

signifies impaired

kidney function.

Lepromin skin test

Used to determine what type of leprosy a person has.

A sample of inactivated leprosy-causing bacteria is injected just under the skin, usually on the forearm, so that a small lump pushes the skin up.

The lump indicates that the antigen has been injected at the correct depth.

The injection site is labelled and examined 3 days, and again 28 days, later to see if there is a reaction.

Medication

Surgical care

Treatment

Medication

Dapsone

RifampinClofazimine

Dapsone

Bactericidal

Mechanism of action is the prevention of

formation of folic acid, inhibiting

bacterial growth

Part of a 2-drug regimen for treatment

of paucibacillary leprosy; part of a 3-

drug regimen for treatment of

multibacillary leprosy

Rifampin

For use in combination with at least 1 other antituberculous drug.

Inhibits DNA-dependent bacterial RNA polymerase.

Cross-resistance may occur. Treat for 6-9 months or until 6 months have elapsed from time of negative sputum test.

Clofazimine

Epidemiology

The number of new cases of leprosy per year (incidence) also

fell from approximately

720,000 in 2000 to about 300,000 in

2005

Since then this has stabilised, with an

estimated 230,000 new cases reported in 2010. The highest numbers of new cases in 2010 were

reported from India, Brazil, Indonesia, the

Democratic Republic of Congo, and Ethiopia

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