LEPROSY

DEFINITION:
 Leprosy is also called as Hansen’s disease.
 It 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 by two polar forms
a. Lepromatous leprosy
b. Tuberculoid leprosy

PROBLEM STATEMENT:
 One of the oldest and most dreaded disease known to mankind.
 Earliest description from India in 600BC
 The prevalence rate has dropped by 90%percent from
21.1cases/10000in 1985to <1/10000in 2000.
 Out of 122 counties only 2 counties still have to reach the elimination
goal brazil and east timor.
 The goal of leprosy elimination at national level as set by national health
policy 2002 had been achieved in the month of December 2005
LEPROSY SITUATION IN INDIA 2012-2013
o A total of 1,35 lac new cases were detected during 2021-2013
o Prevalence was 0.92 lac cases as on 1st April 2013
o Multibacillary cases were 49.92 percent
o Female cases were 37.72 percent children 9.93 percent
o 3.45%cases with visible deformity.
o 33 states /UT’s have already achieved the PR of <1case/10000

CLINICAL FEATURES:
Hypopigmented patches
Partial or total loss of cutaneous sensation in affected areas
Presence of thickened nerves
Presence of acid-fast bacilli in the skin or nasal smears.
SIGNS:
Presence of nodules or lumps especially in the skin of face, ears, plantar ulcers,
loss of fingers or toes, nasal depression, foot drop, claw toes and other
deformities.
EPIDEMIOLOGICAL FACTORS:
1) AGENT:
Mycobacterium leprae
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Acid fast bacilli and occur both as intracellular and extracellular bacilli
Spectrum of clinical presentations
Tuberculoid =borderline tuberculoid=borderline lepromatous=lepromatous
They are characteristically in clumps or bundles called GLOBI.
a)SOURCE OF INFECTION:
It is generally agreed that the multibacillary cases (lepromatous and borderline
lepromatous)
b)PORTAL OF EXIST:
The nose is the major portal of exist.
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.
c)INFECTIVITY:
Highly infective
HOST:
a)AGE:
Leprosy is not particularly a disease of children.
In endemic areas the disease is acquired commonly during childhood.
b)GENDER:
Higher in males than females in most regions of the world.
c)MIGRATION:
Both rural and urban areas
d)IMMUNITY:
Only few persons exposed to infection develop the disease.
A large proportion of early lesions that occur in leprosy heal spontaneously.
e)GENETIC FACTORS: human leucocyte antigen.
ENVIRONMENTAL FACTORS:
Presence of infectious treatment in the environment.
M.leprae remain viable in the dried nasal secretions for 9 days and in moist soil
at room temperature for 46 days.
Overcrowding and lack of ventilation within the household favours
transmission.
a)MODE OF TRANSMISSION:
 Droplet infection (nose)
 Contact transmission (person to person)
 Other routes (insect vectors or by tattooing needles)
b)INCUBATION PERIOD:
3to 5 years (long)
CLASSIFICATION:
INDIAN CLASSIFICATION:
Interdeterminate
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(this denotes those early cases with one or two vague hypo pigmented
macules and definite sensory impairment.
The lesion are bacteriologically negative)
Tuberculoid

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(this type denotes those cases with one or two well defined lesions which may
be flat or raised hypopigmented or erythematous and are anaesthetic.
These lesions are bacteriologically negative.
Borderline
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This type denotes the cases with four or more lesions which may be flat or
raised well or ill defined hypopigmented or erythematous and show sensory
impairment or loss.
The bacteriologically positivity of these lesions is variable.
Without treatment it usually progresses to lepromatous type.
Lepromatous
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This type denotes those cases with diffuse infiltration or numerous flat or
raised, poorly defined shiny, smooth, symmetrically distributed lesions.
The lesions are bacteriologically positive.
Pure neuritic type
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This type denotes those cases of leprosy which show nerve involvement but do
not have any lesions in skin
These cases are bacteriologically negative.
MARTID CLASSIFICATION:
1. Interdeterminate
2. Tuberculoid flat raised
3. Borderline
4. Lepromatous
DIAGNOSIS:
CLINICAL EXAMINATION:
Case taking
 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
 Details of previous history of treatment for leprosy if any
 Presenting complaint or symptom
Physical examination
 A thorough inspection of the body surface to the extent permissible in
good natural light for the presence of suggestive or tell tale evidence of
leprosy.
 Palpation of commonly involved peripheral and cutaneous nerve for the
presence of thickening and or tenderness
Skin biopsy
Nerve biopsy
Lepromin test early reaction, late reaction,
BACTERIAL EXAMINATION:
 Skin smears
 Nasal smears
 Nasal scrapings
Bacterial index (slit skin smear)
Morphological index
Foot pad culture
LEPROSY CONTROL:
 Estimation of the problems
 Case detection
 Multidrug therapy
 Surveillance
 Immunoprophylaxis
 Chemoprophylaxis
  Deformities
 Rehabilitation
 Health education
MULTIDRUG THERAPY:
 Rifampicin
 Dapsone
 Clofazimine
 Ethionamide and protionamide
 Quinolones
 Minocycline
 Clarithromycin

TETANUS
DEFINITION:
An acute disease induced by the exotoxin of clostridium tetani.
Clinically characterised by muscular rigidity which persists throughout illness
punctuated by painful paroxysmal spasms of the voluntary muscles especially
masseters, the facial muscle, the muscle of back and neck
PROBLEM STATEMENT:
EPIDEMIOLOGICAL FACTORS:
1)AGENT:
Clostridium tetani
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Tennis racket or drumstick shape
Spores are highly resistant to a number of injurious agents including boiling,
phenol and autoclaving for 15min at 120 C.
a)RESERVOIR OF INFECTION:
Soil and dust
Also found in the intestine of cattle, horse, goats, sheeps and excreted in feces.
Can survive for years without causing ill effects
Are blown about in dust and occur in wide variety of situations.
b)TOXINS:
When the oxygen level in the surrounding tissue is sufficiently low, the
implanted clostridium tetani spore than germinate into a new, active
vegetative cell that grows and multiplies and most importantly produces
tetanus toxins
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Tetanospasmin (is a neurotoxin)
Tetanolysin (is not believed to be any of the clinical course of tetanus)
The toxin acts on 4 areas
Motor end plates, spinal cord, brain, sympathetic system.
c)PERIOD OF COMMUNICABILITY: none
2)HOST FACTORS:
a)AGE:
It is disease of active age 5-40 yrs. new born baby, female during delivery or
abortion.
b)SEX:
Higher incidence in males than females.
c)OCCUPATION:
Agricultural workers are at high risk.
Incidence of tetanus in urban areas is much lower than in rural areas
d)IMMUNITY: Herd immunity does not protect the individual.
3)ENVIRONMENTAL FACTORS:
Tetanus is a positive environmental hazard.
Depend upon man’s physical and ecological surroundings.
Factors contributing- unhygienic custom habits, unhygienic delivery practices,
ignorance of infection and lack of primary health care services,
a)MODE OF TRANSMISSION:
Trivial pin prick, skin abrasion
Punctured wounds, burns, human bites
Animal bites and stings
Unsterile surgery, IUD
Bowel surgery and dental extraction
Injections, unsterile division of umbilical cord
Compound fractures, otitis media
Chronic skin ulcers, eye infection
Gangrenous limb
b)INCUBATION PERIOD:
Ranges from 3-21 days but can range from day of injury to several months
Average incubation period is 10 days
Depend on character, location and extent of wound,
TYPES OF TETANUS:
Traumatic
Puerperal
Otogenic
Idiopathic
Tetanus neonatorum
Cephalic
PREVENTION:
Tetanus is completely preventable by active tetanus immunization.
Immunization is thought to provide protection for 10 years.
Active immunization
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Combined
Monovalent
COMBINED:
Offered routinely in combination with diphtheria vaccine and killed pertussis
organisms as DPT vaccine.
1st dose -6th week (DPT)
2nd dose- 10th week (DPT)
3rd dose-14th week (DPT)
1st booster-18th month (DPT)
2nd booster-5th completed year (DT)
3rd booster-10th year (TT)
4th booster-16th year (TT)
MONOVALENT VACCINES:
Purified tetanus toxoid (absorbed) supplanted the plain toxoid -higher and
long-lasting immunity response.
Primary course of immunization – 3 doses.
Each of 0.5ml injected into arm given at intervals of 0,2,12 months.
The longer interval between two doses, better is the immune response.
Booster dose: after 5year f/b every 10 year.
Stored between +2 to +8 C and must not be allowed to freeze at any time.
PASSIVE IMMUNIZATON:
Temporary protection-human tetanus immunoglobulin/ATS.
Human tetanus hyperimmunoglobulin:
250-500IU
Produces protective antibody level for atleast 4-weeks
Does not cause serum sickness.
Longer passive protection compared to horse ATS(30days/7-10 days)
Produced at serum institute pune.

FILARIASIS
DEFINITION:
It is a parasitic infection,depend on the host.
Lymphatic filariasis:infection with three nematode worms
 Wucheria bancroti
 Brugi malayi
 Brugi timori
All three infections are transmitted by man by bites of infective
mosquitoes.
The microfilariae circulate in peripheral blood and are available to infect
mosquito vectors when they come to feed.
PROBLEM STATEMENT:
filariasis is a global problem.
It is endemic in many tropical and subtropical countries like
Africa,asia,western pacific and parts of America.
1.4 billion people live in areas with risk of infection
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Out of them 120 million are infected and need treatment
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out of them 40 million people are with overt disease
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15 million people with lymphoedema 25 million men with urogenital
Swelling mainly scrotal hydrocele

Mass drug administration (MDA)of DECwas implemented in india since 2004.

In 2007 the strategy of MDA changed to DEC plus albendazole
In 2012 the prevalence of microfilaria reduced to less than 1% in 192 out of
250 implementation units.
The formal goal of global filariasis programme:
To eliminate the disease in a public health problem
2020 is the informed target date for interrupting transmission.

EPIDEMIOLOGY:

1) AGENT:
There are at least 8 species of filarial parasites that are specific to man.
They are wuchereria bancrofti, brugi malayi, brugia timori,onchocerca
volvulus, loa loa, t perstans, t streptocera, mansonella ozzardi.
Out of these first three causes lymphatic filariasis.
a) PERIODICITY:
Both of the microfilaria of wucheria bancrofti and brugi malayi occurring
in india display nocturna periodicity. i.e., appear large no.at night retreat
from blood stream during the day.
The maximum density Is reported between 10pm to 2 am
This is a biological adaptation to the nocturnal biting habits of vector
mosquitoes.
b) LIFE CYCLE:
definitive host- man interdeterminate host- mosquito
The adult worms are found in the lymphatic system of man where they
may survive for 15 years or more
During their life span after mating female worms give birth to 50,00
immature microfilariae per day into blood circulation via lymphatics . they
may survive up to years or more.
Some of thes microfilariae may be ingested by the mosquitoes during their
blood meal.
C) INCUBATION PERIOD:
The time interval from the invasion of infective larvae to the
development of clinical manifestation.
It is about 8-16 months .
 d) RESERVOIR OF INFECTION:
although filarial infection occurs in animals human filariasis is not
usually a zoonosis.
In man the source of infection is a person with circulating microfilariae
in peripheral blood
2) HOST:
a) AGE: all age are susceptible to infection. In endemic areas ,filarial
infection has been found even in infants aged less than 6 months ago.
Infection rate rise up to the age 20-30 years.
b) SEX: In most endemic areas the microfilariae rate is higher in men,
c) MIGRATION: The movement of people from one place to another has
lead to the extension of filariasis into areas previously non- endemic
d) IMMUNITY: Man may develop resistance to infection only after many
years of exposure.
e) SOCIAL FACTORS: lymphatic filarisis is often associated with
urbanization, industrialization, migration of people, illiteracy, poverty
and poor sanitation.

3) ENVIRONMENTAL FACTORS:
a) CLIMATE: It influences the breeding of mosquitoes their longevity
and the development of parasite in the insect vector. The
temperature was between 22 to 38 degree Celsius and relative
humidity of 70%.
b) DRAINAGE: vectors breed profusely in polluted water,
c) TOWN PLANING: Inadequate sewage disposal and lack of town
planning have aggravated the problems of filariasis in India. The
common breeding places are open ditcges,septic tanks, ill maintained
drains,

VECTORS OF LYMPHATIC FILARIASIS:

In India:
Culex - vector for bancroftian filariasis
Mansonia – vector for brugian filariasis
Culex breeds in polluted water
Mansonia is associated with aquatic plants.
CLINICAL MANIFESTATION:
Only small proportion of infected individual exhibit clinical signs.
There are 2 types
a) Lymphatic filariasis- caused by parasite in lymphatic system.
b) Occult filariasis- due to immune hyper responsiveness of the human
host.

LYMPHATIC FILARIASIS:
It has following stages-
 Asymptomatic amicrofilaremia – does not show microfilariae or
clinical manifestation of the diseases.
 Asymptomatic microfilaremia – asymptomatic, but blood is
positive for microfilariae.
 Stage of acute manifestation: occurs in fist few months and years
Recurrent episodes of acute inflammation in lymph glands and
vessels
Manifested as filarial fever, lymphangitis, lymphadenitis,
lymphoedema and epididymoorchitis(male).
 Stage of chronic obstructive manifestation:
Occurs 10-15 years after the onset of first acute attack.
Causes permanent structural changes due to fibrosis and
obstruction of lymphatic vessel.
Main clinical feature are hydrocele, eleohantasis and chyluria.
In brugian filariasis, genitalia are rarely involved.

OCCULT FILARIASIS:
The classical clinical manifestation are NOT PRESENT and
microfilariae are NOT FOUND in the blood.
Occurs due to hypersensitivity reaction to filarial antigens derived
from mivrofilariae.
Eg: tropical pulmonary eosinophilia.
DIAGNOSIS:
1) Mass blood survey:
It depends upon the demonstration of living parasites in the
human body. Night blood survey are done
 Thick film:
Most commonly used method.
20mm3 of blood is collected from deep finger prick
between 8.30 pm -12 mid night.
The blood flims are dehaemoglobinised, stained,dried,
and examined for microfilariae.
 Membrane filter concentration:
Most sensitive method.
 DEC(Diethyl carbamazepine) provocation test:
Microfilariae can be induced to appear in blood in the
daytime by administering DEC100mg orally.
Microfilariae begin to reach their peak within 15 mibutes
and begin to decrease 2hrs later.
2) SEROLOGICAL TESTS
To detect antibodies in microfilariae and adults using
immunofluroscent and complement fixig techniques.
MANAGEMENT:
1) Treatment for uncomplicated acute dermato
lymphagioadenitis(ADLA)
 Give analgesics – paracetamol (1 g, 3-4times a day)
 Give oral antibiotic -pencilin(1.5g in 3 divided doses X 8
days) in case of allergy to penicillin give oral
erythromycin(1g,3times a day)
 Clean the limb with antiseptic.
 Check for anyb wounds, cuts,abscess(give antibiotic
cream)and interdigital infection give(give antifungal
cream)
 Give advice on prevention of chronic lymphoedema
 Do not give antifilarial medicine
 Home management- elevation of limb , drink plenty of
water, wriggling the toes, washing the limb.
 Follow up after 2 days.
 2) Treatment of severe ADLA:
Refer patient to physician, he iws given
 IV benzylpenicillin (penicillin-G)-3G ,3 times a day until
fever subsides. Then oral phenoxymethylpenicillin
(penicillin v)-750mg to 1g,3 times a dayX 8 Days
 In case of allergy to penicillin,IV erythromycin 1g 3 times
\day until fever subsides
Then oral erythromycin 1g, 3 times a day .
 Give analgesic\antipyretics paracetamol.
 Do not give antifilarial medicine.

HYDROCELE MANAGEMENT:
 The individuals are referred for diagnosis and
surgery done if necessary.
 Men have a good prognosis with early hydrocele
and corrective surgery can be undertaken even
with local anaesthetic.
 Quality pre and post operative care are
important components that help make this
surgery successful. For other genital
damage,more complicated surgery is often
required.
 Unfortunately,however hydrocele surgery is
often too expensive for those afflicted with
lymphatic filariasis.
CONTROL MEASURES:
Even after full regimen of diethylcarbamazine(DEC) some microfilariae still
persisted in the body .so it was difficult to prevent the spread of filariasis
So it is supplemented by effective vector control programme.
The current strategy is based on
 Chemotherapy
 Vector control
CHEMOTHERAPY:
DEC MASS THERAPY

FILARIA CONTROL IN
THE COMMUNITY SELECTIVE TREATMENT

IVERMECTIN DEC-MEDICATED SALT

VECTOR CONTROL
It consists of
 Anti-larval measures
 Anti-adult measures
 Personal prophylaxis
NATIONAL FILARIAL CONTROL PROGRAMME:
 It is operated sice 1955.
 In June 1978 it was merged with malaria scheme,
 Filarial control strategy include:
 Vector control through anti larval operations
 Source reduction
 Detection and treatment of microfilaria carriers
 Morbitity management
The strategy is through
 Annual mass drug administration
 Home based management.