DR. MAHESWARI JAIKUMAR.
maheswarijaikumar2103@gmail.com
LEPROSY
• Leprosy (Hansen’s disease) is a
chronic infectious disease caused
by Mycobacterium leprae.
• It affects mainly the peripheral
nerves.
• It may also affect skin, eyes,
bones, testes and internal
organs.
• The disease manifests itself in
two polar forms.
• 1. LEPROMATOUS LEPROSY. (LL)
• 2. TUBERCULOID LEPROSY. (TL)
• Lying at the two ends of a long
spectrum of the disease, lying
between these two polar types
occur the borderline (BL) and
indeterminate (IL) forms
depending on the host response
to infection
CARDINAL FEATURES
• Leprosy is clinically characterized
by one or more of the following
cardinal features.
• 1. Hypopigmented patches.
• 2. Partial or a total loss of
cutaneous sensation in the
affected areas.
HYPO PIGMENTED PATCH
• 3. Presence of thickened nerves.
• 4. Presence of Acid Fast Bacilli in
the skin or nasal smears.
• The signs of advanced disease
are striking : presence of nodules
or lumps especially in the skin of
the face and ears, plantar ulcers,
loss of fingers or toes, nasal
depression, foot drop, claw toes
and other deformities.
CONTRACTURE
UNTREATED NODULAR
LEPROSY
AGENT
• The agent is Mycobacterium
leprae.
• They are acid fast bacilli, and
occur both as intracellular and
extracellular bacilli.
• They occur characteristically in
clumps or bundles called GLOBI.
• As many as 2 to 7 billion may be
present in one gram of leproma.
• As many as 2 to 7 billion may be
present in one gram of leproma.
SOURCE OF INFECTION
• It is generally agreed that the
multibacillary cases
(lepromatous and boderline
lepromatous cases) are the most
important source of infection.
PORTAL OF EXIT
• The nose is the major portal of
exit.
• Lepromatous cases harbour
millions of M. leprae in their
nasal mucosa which are
discharged when they sneeze or
blow the nose.
• The bacilli can also exit through
ulcerated or broken skin of
bacteriologically positive cases
of leprosy.
INFECTIVITY
• Leprosy is a highly infective disease
but of low pathogenicity.
• An infectious patient can be
rendered non infectious by
treatment with dapsone for about
90 days or with rifampicin for 3
weeks.
• Local application of rifampicin
(drops/spray) might destroy all
the bacteria within 8 days.
ATTACK RATES
• Despite treatment all the cases
have been infectious for long
periods, before treatment is
sought.
HOST FACTORS
AGE
• Leprosy is not particularly a
disease of children.
• An individual can get infected
any time depending upon the
opportunities for exposure.
• In endemic areas, the disease is
acquired commonly during
childhood.
• Incidence rates generally rise to
a peak between 10 to 20 years of
age and then fall.
GENDER
• Both incidence and prevalence
of leprosy appear to be higher in
males than in females in most
regions of the world.
• The excess of cases in males is
attributed to their greater
mobility and increased
opportunities for contact in
many populations.
MIGRATION
• In India leprosy was considered to
be mostly a rural problem.
• But today the disease is equally
found (due to migration of
population) both in rural and urban
areas.
IMMUNITY
• It is a well established fact that
only a few persons exposed to
infection develop the disease.
• A large proportion of early
lesions that occur in leprosy heal
spontaneously.
• Such abortive self healing lesions
suggests immunity acquired
through such lesions.
• A certain degree of immunity is
also probable through infections
with other related mycobacteria.
• Cell-mediated immunity (CMI) is
responsible for resistance to
infection with M.leprae.
• In lepromatous leprosy there is a
complete breakdown of CMI.
GENETIC FACTORS
• Human Lymphocyte Antigen
(HLA) linked genes influence the
type of immune response to the
infection by M. leprae.
ENVIRONMENTAL
FACTORS
• The risk of transmission is
predominantly controlled by
environmental factors. i.e., the
presence of infectious cases in
the environment.
• Humidity favours the survival of
M.leprae in the environment.
• M.leprae can remain viable in
the dried nasal secretions for at
least 9 days and in moist soil at
room temperature for 46 days.
• Overcrowding and lack of
ventilation within the household
favours transmission.
MODE OF TRANSMISSION
• Transmission occurs by:
1. DROPLET INFECTION.
2. CONTACT TRANSMISSION.
3. OTHER ROUTES.
DROPLET INFECTION
• Nose is the most important portal
of exit.
• M.leprae could survive outside
the human host for several hours
or days.
• The organisms are found in large
number in the dried nasal
secretions and they are
discharged in to the environment
as droplets.
CONTACT
TRANSMISSION
• Leprosy is transmitted from
person to person by close
contact between an infectious
patient and a health but
susceptible person.
• This contact may be direct or
indirect (contact with soil, and
fomites ; clothes, linen)
OTHER ROUTES
• Bacilli may also be transmitted by
insect vectors or by tattooing
needles.
• However there is no evidence that
any of these transmission routes is
important in nature.
INCUBATION PERIOD
• Leprosy has a long incubation
period, an average of 3 to 5 years
or more for lepromatous leprosy.
• The tuberculoid leprosy is
thought to have a shorter
incubation period.
• Symptoms can take as long as 20
years to appear.
• Failure to recognize early
symptoms or signs may
contribute to an assumed
prolonged incubation period in
some individuals.
• Some leprologist prefer the term
“latent period” to incubation
period because of the long
duration of the incubation
period.
CLASSIFICATION
• Leprosy is classified based on the
clinical, bacteriological,
immunological and histological
status of patients.
• Indian and Mardid system of
classification are widely used.
INDIAN CLASSIFICATION MARDID CLASSIFICATION
INDETERMINATE INDETERMINATE
TUBERCULOID TUBERCULOID; FLAT;
RAISED
BODERLINE BODERLINE
LEPROMATOUS LEPROMATOUS
PURE NEURITIC TYPE (no
skin lesion)
INDETERMINATE TYPE
• This denotes those early cases
with one or two vague hypo
pigmented macules and definite
sensory impairment.
• The lesions are bacteriologically
negative.
TUBERCULOID TYPE
• This type denotes those cases with
one or two well defined lesions,
which may be flat or raised,
hypopigmented or erythematous
and are anesthetic.
• The lesions are bacterologically
negative.
TESTING FOR CUTANEOUS SENSATION
BODERLINE TYPE
• This type denotes those case
with four or more lesions which
may be flat or raised, well or ill
defined, hypopigmented or
erythematous and show sensory
impairment or loss.
BODERLINE LEPROSY
BODERLINE TYPE
BODERLINE LEPROSY
• The bacteriological positivity of
these lesions is variable.
• Without treatment, it usually
progresses to lepromatous type.
LEPROMATOUS TYPE
• This type denotes those cases with
diffuse infiltration or numerous flat
or raised, poorly defined shiny,
smooth, symmetrically distributed
lesions.
• The lesions are bacterologically
positive.
PURE NEURUTIC TYPE
• This type denotes those cases of
leprosy which show nerve
involvement but do not have any
lesion in skin.
• These cases are bacteriologically
negative.
DIAGNOSIS
• Diagnosis is based on
1. CLINICAL EXAIMINATION.
2. BACTEROLOGICAL
EXAMINATION.
CLINICAL EXAMINATION
• Leprosy is diagnosable on the
basis of proper clinical
examination alone.
• This is called as “case taking”.
• Case taking follows a set pattern,
as follows:
1. INTERROGATION
2. PHYSICAL EXAMINATION
INTERROGATION
• Collection of biodata of the
patient such as name, age,
gender, occupation and place of
residence.
• Family history of leprosy.
• History of contact with leprosy
cases.
• Details of previous history of
treatment for leprosy, if any.
• Presenting complaint or symptom.
PHYSICAL EXAMINATION
• A thorough inspection of the
body surface(skin) to the extent
permissible, in good natural light
for the presence of suggestive,
or tell tale evidence of leprosy.
• Palpation of the commonly involved
peripheral and cutaneous nerve for
the presence of thickening and / or
tenderness.
• They are ulnar nerve near the
median epicondyle, greater
auricular as it turns over the
sternomastoid muscle, lateral
popliteal and the dorsal branch
of the radial nerve.
• Testing for (a) loss of sensation
for heat, cold, pain and light
touch in the skin patches.
• Paresis or paralysis of the
muscles of the hands and feet,
leading to the disabilities or
deformities.
PLANTAR ULCERS
DIAGNOSIS OF LEPROSY
BACTERIOLOGICAL
EXAMINATION
• Bacteriological examination is
done by:
1. SKIN SMEARS.
2. NASAL SMEARS.
3. NASAL SCRAPINGS.
SKIN SMEARS
• Material from the skin is obtained
from an active lesion and also from
one of the ear lobe by the “slit and
scrape method”.
• Conventionally two sites are
examined.
ARTICLES FOR SKIN SMEAR
TESTING
• The skin is cleaned with ether or
spirit and allowed to dry.
• A fold of skin is nipped between
the thumb and the forefinger (of
the left hand in an operator).
FOR SKIN SMEAR
• Enough pressure should be
applied to stop or minimize
bleeding.
• Holding the point of knife vertical
to the apex of the skin fold, it is
pushed into the skin to a depth of
about 2 mm or so, to reach the
dermis.
• A tiny incision is made 5 mm in
length.
• If blood exudes, it should be
wiped off with a small dry
cotton-wool swab.
• The knife blade is rotated
transversely to the line of the cut
90 degrees and the knife point is
used to scrape the first on one
side and then on the other side
of the incision 2 or 3 times to
obtain a tissue pulp from below
the epidermis.
• This material is transferred on to
a glass and spread over an area
of about 8 mm diameter.
• Six smears can conveniently be
made on one microscopic slide.
• The sites of smear should be
accurately recorded so that the
same site can be used for
successive sets of smears made
for assessing the effect of the
treatment.
• The wound is dressed and closed
with a piece of sticking tape
applied over the site.
NASAL SMEARS OR BLOW
• Nasal spray can be best prepared
from the early morning mucus
material.
• The patient is asked to blow his
nose into a clean dry sheet of
cellophane or plastic.
• The smear should be made
straightaway and fixed.
• Nose blowing smears are used
for assessing the patient’s
infectivity.
• In patients with untreated
lepromatous leprosy, nose blow
smears may show a higher
percentage of solid-staining
bacilli than skin smears.
NASAL SCRAPINGS
• An alternative is to use a mucosal
scrapper.
• After going in 4.5cm, the blade is
rotated towards the septum and
scraped a few times and
withdrawn.
• A small ball of cotton is
introduced into the nostril to
absorb any blood that may ooze
out.
Nasal scrapings are not
recommended as a routine.
BACTERIOLOGICAL EXAMINATION
BACTERIAL INDEX
• The BI of the patient is
calculated by adding up the
index from each site examined
and dividing the total by the
number of sites examined.
EXAMPLE
RIGHT
EAR
5+ LEFT EAR 5+
BACK 4+ CHIN 4+
BI = 5+5+4+4 = 18 = 4.5+
4 4
When BI is 3+ and above, at least 25 oil
immersion fields should be examined.
MORPHOLOGICAL INDEX
• The percentage of solid staining
bacilli in a stained smear is
referred to as Morphological
Index. (MI).
FOOT PAD CULTURE
• The only certain way to identify
M.leprae is to inoculate the
material into the foot pads of mice
and demonstrate its multiplication.
• This test is more sensitive than skin
and nasal smears.
TEST FOR DETECTING CMI
LEPROMIN TEST
The test is performed by injecting
intradermally 0.1 ml of lepromin
into the inner aspect of the
forearm of the individual.
• As a routine, the reaction is read
at 48 hours and 21 days.
• Two types of positive reactions
have been described.
EARLY REACTION
• The early reaction is known as
Fernandez reaction.
• A inflammatory response
develops within 24 to 48 hours
and 21 days.
• It is evidenced by redness and
induration at the site of
inoculation.
• If the diameter of the red area is
more than 10mm at the end of
48 hours, the test is considered
positive.
• The early positive reaction
indicates whether or not a
person has been previously
sensitized by exposure to and
infection by the leprosy bacilli.
• This reaction is similar to that of
mantoux test for TB.
LATE REACTION
• This is the classical Mitsuda
reaction.
• The reaction develops late,
becomes apparent in 7-10 days
following the injection and
reaching its maximum in 3 t0 4
weeks.
• The test is read at 21 days.
• At the end of 21 days, if there is
a nodule more than 5mm in
diameter at the site of
inoculation, the reaction is said
to be positive.
• The late reaction by the bacillary
component of the antigen
indicates CMI.
• Lepromin test is not a diagnostic
test. The test is a useful tool in
evaluating the immune status.
LEPROSY CONTROL
• Can be achieved through :
1. Estimation of the problem.
2. Case detection.
3. Multidrug therapy.
4. Surveillance.
• 5. immunoprophylaxis.
• 6. Chemoprophylaxis.
• 7. Deformities.
• 8. Rehabilitation.
• 9. Health education.
MULTIDRUG THERAPHY
• The following drugs are used in
the management of leprosy.
1. Rifampicin.
2. Dapsone.
3. Clofazimine.
4. Ethionamide and
protionamide.
5. Quinolones.
6. Minocycline.
7. Clarithromycin.
REGIMENS OF
CHEMOTHERAPHY BY
WHO
CHEMOTHERAPHY
FOR ADULTS
FOR MULTIBACILLARY LEPROSY
• RIFAMPICIN 600 mg, once
monthly given under supervision.
• DAPSONE 100 mg daily, self
administered.
• CLOFAZIMINE 300 mg, once
monthly supervised; and 50 mg
daily, self administered.
• When clofazimine is
unacceptable owing to the
colouration of the skin
ETHIONAMIDE 250 to 375 mg
self administered daily doses is
suggested.
FOR PAUCIBACILLARY LEPROSY
• RIFAMPICIN 600 mg once a
month, supervised
• DAPSONE 100 mg (1-2 mg/kg of
body weight) daily, self
administered
CHEMOTHERAPHY FOR
CHILDREN (10 – 14 YEARS)
MULTIBACILLARY LEPROSY
• RIFAMPICIN 450 mg, once a
month, given under supervision.
• DAPSONE 50 mg, self
administered.
• CLOFAZIMINE 150 mg once a
month supervised; and 50 mg
every other day.
PAUCIBACILLARY LEPROSY
• RIFAMPICIN 450 mg once a
month supervised.
• DAPSONE 50 mg, daily, self
administered.
• Children under the age of 10
years should receive
appropriately reduced doses of
the above drugs.
DUARATION OF TREATMENT
• The treatment duration varies
according to the type of disease.
• The recommendations are as
follows
MULTIBACILLARY
• MB blister
packs for 12
months, within
18 months.
PAUCIBACILLARY
• PB blister
packs for 6
months, within
9 months.
COMMUNITY SENSITIZATION
THANK YOU

EPIDEMIOLOGY OF LEPROSY

  • 1.
  • 2.
    LEPROSY • Leprosy (Hansen’sdisease) is a chronic infectious disease caused by Mycobacterium leprae.
  • 3.
    • It affectsmainly the peripheral nerves. • It may also affect skin, eyes, bones, testes and internal organs.
  • 4.
    • The diseasemanifests itself in two polar forms. • 1. LEPROMATOUS LEPROSY. (LL) • 2. TUBERCULOID LEPROSY. (TL)
  • 5.
    • Lying atthe two ends of a long spectrum of the disease, lying between these two polar types occur the borderline (BL) and indeterminate (IL) forms depending on the host response to infection
  • 7.
    CARDINAL FEATURES • Leprosyis clinically characterized by one or more of the following cardinal features.
  • 8.
    • 1. Hypopigmentedpatches. • 2. Partial or a total loss of cutaneous sensation in the affected areas.
  • 9.
  • 10.
    • 3. Presenceof thickened nerves. • 4. Presence of Acid Fast Bacilli in the skin or nasal smears.
  • 11.
    • The signsof advanced disease are striking : presence of nodules or lumps especially in the skin of the face and ears, plantar ulcers, loss of fingers or toes, nasal depression, foot drop, claw toes and other deformities.
  • 12.
  • 13.
  • 15.
    AGENT • The agentis Mycobacterium leprae. • They are acid fast bacilli, and occur both as intracellular and extracellular bacilli.
  • 18.
    • They occurcharacteristically in clumps or bundles called GLOBI. • As many as 2 to 7 billion may be present in one gram of leproma.
  • 19.
    • As manyas 2 to 7 billion may be present in one gram of leproma.
  • 20.
    SOURCE OF INFECTION •It is generally agreed that the multibacillary cases (lepromatous and boderline lepromatous cases) are the most important source of infection.
  • 21.
    PORTAL OF EXIT •The nose is the major portal of exit. • Lepromatous cases harbour millions of M. leprae in their nasal mucosa which are discharged when they sneeze or blow the nose.
  • 22.
    • The bacillican also exit through ulcerated or broken skin of bacteriologically positive cases of leprosy.
  • 23.
    INFECTIVITY • Leprosy isa highly infective disease but of low pathogenicity. • An infectious patient can be rendered non infectious by treatment with dapsone for about 90 days or with rifampicin for 3 weeks.
  • 24.
    • Local applicationof rifampicin (drops/spray) might destroy all the bacteria within 8 days.
  • 25.
    ATTACK RATES • Despitetreatment all the cases have been infectious for long periods, before treatment is sought.
  • 26.
  • 27.
    AGE • Leprosy isnot particularly a disease of children. • An individual can get infected any time depending upon the opportunities for exposure.
  • 28.
    • In endemicareas, the disease is acquired commonly during childhood. • Incidence rates generally rise to a peak between 10 to 20 years of age and then fall.
  • 29.
    GENDER • Both incidenceand prevalence of leprosy appear to be higher in males than in females in most regions of the world.
  • 30.
    • The excessof cases in males is attributed to their greater mobility and increased opportunities for contact in many populations.
  • 31.
    MIGRATION • In Indialeprosy was considered to be mostly a rural problem. • But today the disease is equally found (due to migration of population) both in rural and urban areas.
  • 32.
    IMMUNITY • It isa well established fact that only a few persons exposed to infection develop the disease.
  • 33.
    • A largeproportion of early lesions that occur in leprosy heal spontaneously. • Such abortive self healing lesions suggests immunity acquired through such lesions.
  • 34.
    • A certaindegree of immunity is also probable through infections with other related mycobacteria. • Cell-mediated immunity (CMI) is responsible for resistance to infection with M.leprae.
  • 36.
    • In lepromatousleprosy there is a complete breakdown of CMI.
  • 37.
    GENETIC FACTORS • HumanLymphocyte Antigen (HLA) linked genes influence the type of immune response to the infection by M. leprae.
  • 38.
  • 39.
    • The riskof transmission is predominantly controlled by environmental factors. i.e., the presence of infectious cases in the environment. • Humidity favours the survival of M.leprae in the environment.
  • 40.
    • M.leprae canremain viable in the dried nasal secretions for at least 9 days and in moist soil at room temperature for 46 days. • Overcrowding and lack of ventilation within the household favours transmission.
  • 41.
    MODE OF TRANSMISSION •Transmission occurs by: 1. DROPLET INFECTION. 2. CONTACT TRANSMISSION. 3. OTHER ROUTES.
  • 42.
    DROPLET INFECTION • Noseis the most important portal of exit. • M.leprae could survive outside the human host for several hours or days.
  • 43.
    • The organismsare found in large number in the dried nasal secretions and they are discharged in to the environment as droplets.
  • 44.
    CONTACT TRANSMISSION • Leprosy istransmitted from person to person by close contact between an infectious patient and a health but susceptible person.
  • 45.
    • This contactmay be direct or indirect (contact with soil, and fomites ; clothes, linen)
  • 46.
    OTHER ROUTES • Bacillimay also be transmitted by insect vectors or by tattooing needles. • However there is no evidence that any of these transmission routes is important in nature.
  • 47.
    INCUBATION PERIOD • Leprosyhas a long incubation period, an average of 3 to 5 years or more for lepromatous leprosy. • The tuberculoid leprosy is thought to have a shorter incubation period.
  • 48.
    • Symptoms cantake as long as 20 years to appear. • Failure to recognize early symptoms or signs may contribute to an assumed prolonged incubation period in some individuals.
  • 49.
    • Some leprologistprefer the term “latent period” to incubation period because of the long duration of the incubation period.
  • 50.
    CLASSIFICATION • Leprosy isclassified based on the clinical, bacteriological, immunological and histological status of patients. • Indian and Mardid system of classification are widely used.
  • 52.
    INDIAN CLASSIFICATION MARDIDCLASSIFICATION INDETERMINATE INDETERMINATE TUBERCULOID TUBERCULOID; FLAT; RAISED BODERLINE BODERLINE LEPROMATOUS LEPROMATOUS PURE NEURITIC TYPE (no skin lesion)
  • 54.
    INDETERMINATE TYPE • Thisdenotes those early cases with one or two vague hypo pigmented macules and definite sensory impairment. • The lesions are bacteriologically negative.
  • 55.
    TUBERCULOID TYPE • Thistype denotes those cases with one or two well defined lesions, which may be flat or raised, hypopigmented or erythematous and are anesthetic. • The lesions are bacterologically negative.
  • 56.
  • 58.
    BODERLINE TYPE • Thistype denotes those case with four or more lesions which may be flat or raised, well or ill defined, hypopigmented or erythematous and show sensory impairment or loss.
  • 59.
  • 61.
  • 62.
  • 63.
    • The bacteriologicalpositivity of these lesions is variable. • Without treatment, it usually progresses to lepromatous type.
  • 64.
    LEPROMATOUS TYPE • Thistype denotes those cases with diffuse infiltration or numerous flat or raised, poorly defined shiny, smooth, symmetrically distributed lesions. • The lesions are bacterologically positive.
  • 67.
    PURE NEURUTIC TYPE •This type denotes those cases of leprosy which show nerve involvement but do not have any lesion in skin. • These cases are bacteriologically negative.
  • 69.
    DIAGNOSIS • Diagnosis isbased on 1. CLINICAL EXAIMINATION. 2. BACTEROLOGICAL EXAMINATION.
  • 70.
    CLINICAL EXAMINATION • Leprosyis diagnosable on the basis of proper clinical examination alone. • This is called as “case taking”.
  • 71.
    • Case takingfollows a set pattern, as follows: 1. INTERROGATION 2. PHYSICAL EXAMINATION
  • 72.
    INTERROGATION • Collection ofbiodata of the patient such as name, age, gender, occupation and place of residence. • Family history of leprosy.
  • 73.
    • History ofcontact with leprosy cases. • Details of previous history of treatment for leprosy, if any. • Presenting complaint or symptom.
  • 74.
    PHYSICAL EXAMINATION • Athorough inspection of the body surface(skin) to the extent permissible, in good natural light for the presence of suggestive, or tell tale evidence of leprosy.
  • 75.
    • Palpation ofthe commonly involved peripheral and cutaneous nerve for the presence of thickening and / or tenderness.
  • 76.
    • They areulnar nerve near the median epicondyle, greater auricular as it turns over the sternomastoid muscle, lateral popliteal and the dorsal branch of the radial nerve.
  • 77.
    • Testing for(a) loss of sensation for heat, cold, pain and light touch in the skin patches. • Paresis or paralysis of the muscles of the hands and feet, leading to the disabilities or deformities.
  • 78.
  • 79.
  • 80.
    BACTERIOLOGICAL EXAMINATION • Bacteriological examinationis done by: 1. SKIN SMEARS. 2. NASAL SMEARS. 3. NASAL SCRAPINGS.
  • 81.
    SKIN SMEARS • Materialfrom the skin is obtained from an active lesion and also from one of the ear lobe by the “slit and scrape method”. • Conventionally two sites are examined.
  • 82.
    ARTICLES FOR SKINSMEAR TESTING
  • 84.
    • The skinis cleaned with ether or spirit and allowed to dry. • A fold of skin is nipped between the thumb and the forefinger (of the left hand in an operator).
  • 85.
  • 87.
    • Enough pressureshould be applied to stop or minimize bleeding. • Holding the point of knife vertical to the apex of the skin fold, it is pushed into the skin to a depth of about 2 mm or so, to reach the dermis.
  • 88.
    • A tinyincision is made 5 mm in length. • If blood exudes, it should be wiped off with a small dry cotton-wool swab.
  • 89.
    • The knifeblade is rotated transversely to the line of the cut 90 degrees and the knife point is used to scrape the first on one side and then on the other side of the incision 2 or 3 times to obtain a tissue pulp from below the epidermis.
  • 90.
    • This materialis transferred on to a glass and spread over an area of about 8 mm diameter. • Six smears can conveniently be made on one microscopic slide.
  • 91.
    • The sitesof smear should be accurately recorded so that the same site can be used for successive sets of smears made for assessing the effect of the treatment.
  • 92.
    • The woundis dressed and closed with a piece of sticking tape applied over the site.
  • 93.
    NASAL SMEARS ORBLOW • Nasal spray can be best prepared from the early morning mucus material. • The patient is asked to blow his nose into a clean dry sheet of cellophane or plastic.
  • 94.
    • The smearshould be made straightaway and fixed. • Nose blowing smears are used for assessing the patient’s infectivity.
  • 95.
    • In patientswith untreated lepromatous leprosy, nose blow smears may show a higher percentage of solid-staining bacilli than skin smears.
  • 96.
    NASAL SCRAPINGS • Analternative is to use a mucosal scrapper. • After going in 4.5cm, the blade is rotated towards the septum and scraped a few times and withdrawn.
  • 97.
    • A smallball of cotton is introduced into the nostril to absorb any blood that may ooze out. Nasal scrapings are not recommended as a routine.
  • 98.
  • 100.
  • 101.
    • The BIof the patient is calculated by adding up the index from each site examined and dividing the total by the number of sites examined.
  • 102.
    EXAMPLE RIGHT EAR 5+ LEFT EAR5+ BACK 4+ CHIN 4+ BI = 5+5+4+4 = 18 = 4.5+ 4 4 When BI is 3+ and above, at least 25 oil immersion fields should be examined.
  • 103.
    MORPHOLOGICAL INDEX • Thepercentage of solid staining bacilli in a stained smear is referred to as Morphological Index. (MI).
  • 104.
    FOOT PAD CULTURE •The only certain way to identify M.leprae is to inoculate the material into the foot pads of mice and demonstrate its multiplication. • This test is more sensitive than skin and nasal smears.
  • 105.
    TEST FOR DETECTINGCMI LEPROMIN TEST The test is performed by injecting intradermally 0.1 ml of lepromin into the inner aspect of the forearm of the individual.
  • 106.
    • As aroutine, the reaction is read at 48 hours and 21 days. • Two types of positive reactions have been described.
  • 107.
    EARLY REACTION • Theearly reaction is known as Fernandez reaction. • A inflammatory response develops within 24 to 48 hours and 21 days.
  • 108.
    • It isevidenced by redness and induration at the site of inoculation. • If the diameter of the red area is more than 10mm at the end of 48 hours, the test is considered positive.
  • 109.
    • The earlypositive reaction indicates whether or not a person has been previously sensitized by exposure to and infection by the leprosy bacilli. • This reaction is similar to that of mantoux test for TB.
  • 110.
    LATE REACTION • Thisis the classical Mitsuda reaction. • The reaction develops late, becomes apparent in 7-10 days following the injection and reaching its maximum in 3 t0 4 weeks.
  • 111.
    • The testis read at 21 days. • At the end of 21 days, if there is a nodule more than 5mm in diameter at the site of inoculation, the reaction is said to be positive.
  • 112.
    • The latereaction by the bacillary component of the antigen indicates CMI. • Lepromin test is not a diagnostic test. The test is a useful tool in evaluating the immune status.
  • 113.
    LEPROSY CONTROL • Canbe achieved through : 1. Estimation of the problem. 2. Case detection. 3. Multidrug therapy. 4. Surveillance.
  • 114.
    • 5. immunoprophylaxis. •6. Chemoprophylaxis. • 7. Deformities. • 8. Rehabilitation. • 9. Health education.
  • 115.
    MULTIDRUG THERAPHY • Thefollowing drugs are used in the management of leprosy. 1. Rifampicin. 2. Dapsone. 3. Clofazimine.
  • 117.
    4. Ethionamide and protionamide. 5.Quinolones. 6. Minocycline. 7. Clarithromycin.
  • 118.
  • 120.
  • 121.
    FOR MULTIBACILLARY LEPROSY •RIFAMPICIN 600 mg, once monthly given under supervision. • DAPSONE 100 mg daily, self administered. • CLOFAZIMINE 300 mg, once monthly supervised; and 50 mg daily, self administered.
  • 122.
    • When clofazimineis unacceptable owing to the colouration of the skin ETHIONAMIDE 250 to 375 mg self administered daily doses is suggested.
  • 123.
    FOR PAUCIBACILLARY LEPROSY •RIFAMPICIN 600 mg once a month, supervised • DAPSONE 100 mg (1-2 mg/kg of body weight) daily, self administered
  • 125.
  • 126.
    MULTIBACILLARY LEPROSY • RIFAMPICIN450 mg, once a month, given under supervision. • DAPSONE 50 mg, self administered. • CLOFAZIMINE 150 mg once a month supervised; and 50 mg every other day.
  • 127.
    PAUCIBACILLARY LEPROSY • RIFAMPICIN450 mg once a month supervised. • DAPSONE 50 mg, daily, self administered. • Children under the age of 10 years should receive appropriately reduced doses of the above drugs.
  • 128.
    DUARATION OF TREATMENT •The treatment duration varies according to the type of disease. • The recommendations are as follows
  • 129.
    MULTIBACILLARY • MB blister packsfor 12 months, within 18 months.
  • 130.
    PAUCIBACILLARY • PB blister packsfor 6 months, within 9 months.
  • 132.
  • 133.