Development of Urinary Tract & Common Abnormalities

Evolution of Kidney Development (3 stages)

Note the image: pronephric system are at the superior (cervical region) portion, mesonephric system at the middle portion and the metanephric system at the inferior (sacral region) portion of the embryo)

Mesonephric duct opens into the urogenital sinus.

Yellow: endodermal (gut)
Blue: intermediate mesoderm (kidney & genital)

Each vertebrate’s excretory system develop:

  • filtration units
  • nephric duct (connected to filtration unit)

1) Pronephros (1 pair of kidneys)

  • lowest verterbrates have 1 pair of kidneys
  • a few nephrons (filtration unit) connected to an unbranched pronephric duct
  • totally disappear at birth (human)

2) Mesonephros

  • More advanced classes (fish, amphibian)
  • A second pair of kidneys
  • linear array of nephrons (filtration unit) connected to an unbranced mesonephric duct
  • May remain at birth (part of male reproductive tract)


  • Amniote classes (reptiles, birds, mammals, humans)
  • Adult life human kidney


As mentioned above, the urinary & genital system both develop from: intermediate mesoderm (along the posterior abdominal wall)

The pronephros
During 4th week, pronephros appear at the cervical region.
By the end of 4th week, pronephros disappears.

Note the intermediate column:
intermediate mesoderm where the urinary & genital system are derived from

Note the:

  • Pronephric tubule
  • Primary Nephric duct
  • Glomus (primitive glomerulus)

The mesonephros
At the end of 4th week, during the regression of the pronephros, the 1st tubules of mesonephros starts to appear.
By middle of 2nd month, a large mesonephros is visible.Then, the cranial tubules gradually starts degenerating.
By the end of 2nd month, most of the mesonephros disappears, but the mesonephric duct remains (only in males)

Note the intermediate mesoderm

Note the:

  • Bowman’s capsule
  • Mesonephric tubule
  • Mesonephric duct
  • Glomerulus

The pronephric components disappear.

The metanephrous
During the 5th week, the metanephros/permanent kidney appears in the sacral region of the intermediate mesoderm.


  • Mesonehpric duct
  • Urogenital sinus
  • Ureteric bud

The mesonephric duct opens into the urogenital sinus.
The ureteric bud is an outgrowth from the mesonephric duct. The ureteric bud joins the metanephric blastema (also known as metanephros).


  • Urogenital septum
  • Cloaca
  • Allantois

Portion of the hindgut (yellow) incorporated into the umbilical cord is known as the: Allantois.

Postallantoic part of the hindgut is called the: Cloaca.

The urorectal septum divides the hindgut (cloaca) into:

  • Dorsal : anorectal canal (the ASS)
  • Ventral: urogenital sinus (where the mesonephric duct opens into)

This is a pig embryo, note the location of the mesonephros & metanephros relative to one another.


This image depicts the development of the metanephros to the adult kidney.
Note the ureteric bud: Dark pink

The ureteric bud elongates and become separate from the mesonephric duct (green), and is now opening into the vesico-urethral canal (pink) -> future urinary bladder.

The ureteric bud goes on penetrating the metanephric tissue (orange). The bud then dilates and forms the renal pelvis -> splits into branches (major calyces) -> each calyx forms 2 buds -> each bud forms 12/more generation of branching (2nd, 3rd, 4th orders forming the minor calyces) (1st, 5-12th orders forming the 1-3 millions of collecting tubules).

Therefore, the ureteric bud will develop the:

  • Minor & major calyx
  • Collecting Tubule
  • Collecting duct
  • Ureter


Note the:

  • Metanephric tissue caps
  • Renal vesicle


The metanephric mesoderm/metanephros/metanephric blastema at the end of collecting tubule are shaped in a way forming the metanephric tissue cap/metanephric mass, which will be induced by the collecting tubule to form nephrons. This metanephric tissue cap will form cell clusters, and lumen will then be formed within the cell clusters forming renal vesicle (metanephric vesicle). The renal vesicle will form a S-shaped tubule which will then develop into the bowman’s capsule. Capillaries will grow at the other end, forming glomerulus, whereby the Bowman’s capsule will fit around it. The tubules + glomerulus forms a nephron. Then the tubules of the nephron lengthen and forms the PCT, Loop of Henle & DCT.
Therefore, the metanephros will develop the:
  • Bowman’s capsule
  • PCT
  • Loop of Henle
  • DCT


*IMPORTANT FOR EXAM: The permanent kidney:

Note the regions of the functional kidney derived from the metanephric mesoderm & ureteric bud.

1) Mesonephros/metanephric blastema/metanephric mesoderm:

  • Bowman’s Capsule
  • Proximal Convoluted kidney
  • Loop of Henle
  • Distal Convoluted Kidney

2) Ureteric Bud:

  • Minor & major calyx
  • Collecting Tubule
  • Collecting duct
  • Ureter

20 nephrons open into 1 collecting tubule.

As we already know, the ureteric bud is connected with the metanephric blastema/metanephros. (which the resulting collecting duct formed from the ureteric bud will induce the metanephros to form the renal vesicles). IF the ureteric bud for some reason fails to contact/connect or induce the metanephric blastema -> then the fetus will suffer from Congenital Polycystic Kidney (numerous collecting ducts surrounded by cysts/undifferentiated cells of the metanephros). There are 2 types:

1) Autosomal dominant 

  • Cysts from ALL parts of nephron
  • More common
  • Renal failure during adulthood

2) Autosomal recessive

  • Multiple cysts from collecting tubule
  • Progressive disorder
  • Renal failure in infancy 


It’s our genes that controls the formation of growth factors and determines whether the kidney develops normally or not.
It requires the epithelial-mesenchyme interaction. The signaling between these two different tissues is required to form the functional unit of the systems in which it is used.
The differentiation of the kidney involves the:
  • WT1 Transcription gene (expressed by the metanephrous mesoderm) via the GDNF & HGF Growth factors

It makes the tissue component differentiate & form the nephrons (in response to the ureteric bud induction via FGF-2, BMP-7 Growth Factors).

Mutation in WT1 gene produces abnormal differention, causing -> Wilm’s Tumour.

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Hi everyone!

It’s been sometime since I’ve updated this medical blog. I hope it has served you well in your medical studies as much as it did for myself. Good news, I have completed my phase 1 medical studies (MBBS) or equivalent to USMLE Step 1.

Due to my hectic schedule, I haven’t managed to put on a better template for this blog. It also seems that the Google Site Search’s pretty messed up as well. However, lookout for a major revamp soon! I will try to make this blog more user friendly, so that lecture notes can be easily found.

So far, there are basic sciences lecture notes on all organ systems except Cardiovascular, Respiratory, Haematology and Gastrointestinal Systems. That will probably take some time for me to update, probably after the blog revamp. I will also be starting off a mailing list and twitter account so that you guys can get notified for any updates as well as quiz and tips!


Here’s my blog analytics from 8th February to 6th March 2011:


My blog’s average is around 4,000 uniques per week and can reach up til 20,000 uniques per month. These are from returning visitors as well as referred first time visitors from search engines and other sites.


61% of visitors are from the United States – so the syllabus covered in this blog is relevant to USMLE students as well.

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Behavioural response to exercise

Topics covered:

  • Problems with sedentary lifestyle
  • Benefits of changing lifestyle
    • enhance daily function
    • maintain reserve capacities
    • prevent diseases
      • diabetes
      • osteoarthritis
      • heart disease
    • decrease effects of age and chronic diseases
  • Hazards of strenuous exercise
    • heart attack
    • amenorrhea
    • osteoporosis
    • infertility
    • suppresses immune system (when already sick)
    • back & shoulder pain
    • dehydration
    • hyperthermia (overheat – heat stroke)
    • injury from high impact exercises
  • Prevention of problems with strenuous exercise
    • Appropriate footwear
    • improving coordination
    • alternate easy & harder workouts
    • warm up, cool down
    • stretching
    • take days off
    • food rich in antioxidants (Vit. A, C & E)
  • Risk factors – strenuous exercises
    • Asthma
    • Cystic fibrosis
    • Diabetes

Impairment & disability


  • any loss or abnormality of psychological, physiological or anatomical structure or function


  • any restriction or lack (resulting from an impairment) of ability to perform an activity
    • in the manner or within the range considered normal for a human being


  • disadvantage for a given individual, resulting from an impairment or a disability,
    • that prevents the fulfillment of a role that is considered normal (depending on age, sex and social and cultural factors) for that individual

Nature of disability

  • Time of onset
    • infancy
    • later in life
  • Functions impaired
  • Severity of disability
  • Visibility of disability
  • Stability of disability
  • Pain

Stages of accommodation

COHN’S 5 stages in adjustment process

  1. Shock
  2. Expectancy of recovery
  3. Mourning
  4. Defence
  5. Final adjustment

Stages of family adjustment (response to child’s disability)

  1. Withdrawal/rejection
  2. Denial
  3. Fear & frustration
  4. Adjustment

Devaluation of disability – Why?

  1. Attitudinal barrier
  2. Overvaluation of physique
  3. Blaming the victim
  4. Insistence of mourning


Many persons with disabilities-feel-their problems stems primarily from

  • prejudice
  • discrimination


  • Name-calling by non-disabled person

Pathology of peripheral neuropathies

Tests for peripheral neuropathy

  • Electromyography
    • measures electrical impulses in muscle at rest & when contracting
    • Differentiates between muscle and nerve disorders
  • Nerve conduction velocity
    • assess the degree of damage in the larger nerve fibres due to myelin loss
    • Slow transmission –> myelin damage
    • Decrease strength of impulse -> axonal degeneration
  • Nerve biopsy
    • invasive
    • sural nerves (unmyelinated nerve)
  • Skin biopsy
    • assess damage present in small fibres
    • nerve conduction tests cannot assess these

Approach to peripheral nerve diseases

Consider whether the pathology is:

  • Primary damage to Schwann cells/myelin
    • Acute inflammatory demyelinating polyradiculoneuropathy (GBS)
    • Chronic inflmamatory demyelinating polyradiculoneuropath
    • Paraprotein neuropathy
    • Charcot-Marie-Tooth type 1
  • Damage to neuron/axon
    • Damage affecting predominantly small unmyelinated fibres
      • amyloid
      • diabetes mellitus
      • HIV
    • Affecting all axonal population
      • vasculitis
      • CMT type 2

Pathology of demyelination

  • Axon damaged
  • Neural bodies intact
  • Conduction block
    • conduction velocity decreases

Patterns of axonal pathology

  1. Wallerian degeneration
    • In transected axon
      • distal portion undergoes disintegration & degradation
    • Limited recovery & regeneration
    • Neuronal body
      • chromatolysis
        • activation of protein synthesis to help regenerate axon
    • Examples:
      • trauma
      • infarction
        • diabetic mononeuropathy
        • vasculitis
      • neoplastic infiltration
  2. Distal axonopathy
    • Degeneration of axon and myelin starts in the most distal part of the axon
    • Axon dies back (retrograde)
      • ‘stocking-glove’ sensory
      • motor deficit
    • Caused by neuronal body pathology
      • resulting in inability to sustain the metabolic needs of the axon
    • Examples
      • drugs
      • toxins
      • organophosphates
      • diabetic polyneuropathy*
      • alcohol
      • vitamin deficiency
      • uraemia
      • malignancy

Classification of peripheral neuropathy

By etiology

  1. Inflammatory neuropathies
    • Immune-mediated
    • Examples
      • Gullain-Barre Syndrome
      • chronic inflammatory demyelinating polyradiculoneuropathy
  2. Infectious
    • Examples
      • Leprosy (Hansen’s disease)
      • Diptheria
      • Varicella-zoster
  3. Hereditary
    • Examples
      • Charcot-Marie-Tooth 1,2 and X
  4. Acquired metabolic & toxic neuropathies
    • Examples
      • Diabetes mellitus
      • vitamin deficiency
      • liver disease
      • alcohol
      • malignancy
      • paraneoplastic

By site of pathology

  • Affecting Schwann cells/myelin
    • Acute inflammatory demyelinating polyradiculoneuropathy (GBS)
    • Chronic inflmamatory demyelinating polyradiculoneuropathy
    • Paraprotein neuropathy
    • Charcot-Marie-Tooth type 1
  • Affecting the neurons/axons
    • Damage affecting predominantly small unmyelinated fibres
    • Example
      • Amyloid
      • Diabetes mellitus
      • HIV
  • Affecting all axonal population
    • Vasculitis
    • CMT type 2



Acute inflammatory demyelinating polyradiculoneuropathy

  • General
    • Also known as: Guillain-Barre Syndrome
    • T-cell mediated immune response & humoral response
  • Clinical features
    • Rapidly evolving
      • Ascending symmetrical weakness
      • Areflexia
    • Variable autonomic dysfunction
    • Mild sensory sign
    • Mostly preceded by an acute flu-like illness
      • complication of influenzae infection
  • Important features
    • Ascending paralysis
    • Loss of deep tendon reflexes
    • Decreased nerve conduction
    • Increase in CSF protein
      • Little cell increase
  • Infectious agents implicated include
    • Campylobacter jejuni
    • CMV
    • EBV
    • Mycoplasma pneumoniae
    • Influenzae virus
  • Microscopic pathology picture:
    • Endoneurial lymphocytic inflammation
      • macrophage infiltration
    • More severe in the nerve roots
      • more subtle in the periphery
      • Axonal damage when disease is severe
    • Electron microscopy
      • macrophage penetrating basement membrane of Schwann cells
      • Stripping myelin sheath away
      • Remyelination can occur
  • Plasmapharesis is effective in some cases


Chronic inflmamatory demyelinating polyradiculoneuropathy

  • Classical Triad
    • Symmetrical proximal & distal weakness
      • for more than 2 months
    • Loss of large fibre modalities
    • Loss of deep tendon reflexes
  • Laboratory studies
    • Endoneurial inflammation
    • Onion-bulb formation in semithin sections
      • due to repeated demyelination & remyelination

Hereditary Sensory and Motor Neuropathy (HSMN)

  • General
    • Also known as Charcot-Marie-Tooth type 1
  • Clinical features
    • Slowly progressive distal weakness
    • Usually begin in childhood
    • Muscle atrophy and sensory impairment
    • Dominance of distal lower extremities signs and symptom
    • Hammertoes
    • Pes caves
      • high arch
    • Nerve enlargement (hypertrophy)
      • If nerves palpable and tremors = CMT type 1
    • Very slow disease with normal longevity
  • Pathology
    • Decrease numbers of large & small myelinated fibres
    • Onion bulb formation
    • Increase in calibre of affected nerves
      • nerve hypertrophy
    • Axonal form (CMT2)
      • no onion bulb, but regenerative axonal clusters
    • Genetic mutation of myelin related proteins

Paraprotein neuropathy


  • Neuropathy associated with a monoclonal gammopathy
  • Incidence
    • > 50 yrs
    • male
  • Clinical features
    • Mild slowly progressive symmetrical distal weakness
    • Painful with severe sensory loss & paresthesia
  • Diagnosis
    • Monoclonal IgM with anti-MAG (myelin-associated glycoprotein activity)
  • Pathology
    • Non-specific myelin & axonal loss
    • POEMS syndrome
      • polyneuropathy
      • organomegaly
      • endocrinopathy
      • M protein
      • skin changes



Amyloid neuropathy

  • General
    • Hereditary/acquired
  • Important features
    • Small fibre neuropathy
      • pain
      • temperature
      • autonomic dysfunction*
  • Clinical features
    • Painful dysesthesias
    • Bowel & bladder dysfunction
    • Impotence
    • Orthostasis
    • Cardiac & renal abnomalites
  • Pathology
    • Biopsy abdominal fatpad
      • Amyloid deposition in endomerium & vascular wall
      • Large myelinated fibres are preserved


Diabetic polyneuropathy

  • Cause
    • diabetes mellitus
  • Most common pattern
    • length-dependent axonal sensorimotor polyneuropathy
  • Manifest as
  • Clincal features
    • Start in distal lower extremities
      • longest nerve fibres
    • Gait abnormality
    • Autonomic abnormality
      • ‘diabetic autonomic neuropathy
    • Sensory dysfunction distal extremity
      • glove & stocking numbness
    • weakness of distal lower extremity
  • Pathology
    • Axonal neuropathy
    • Loss of large, small & unmyelinated fibres
    • Entirely NON-SPECIFIC
  • Pathophysiology
    • Nerve ischaemia
      • due to diabetic microangiopathy
      • poor blood flow
      • may easily develop ulceration


  • Skin biopsy to assess small-nerve fibres
    • Easy to perform
    • Provides information on small nerve fibres
      • not possible with sural nerve biopsy
      • nor with routine neurophysiological testing
    • Can demonstrate subclinical neuropathy
      • eg. in diabetic patients



Hansen’s disease

  • Causal organism
    • Mycobacterium leprae
  • Pathology
    • In Lepromatous leprosy
      • Schwann cells are invaded by the mycobacteria
      • Increase in Th2 cytokines: IL3, IL5, IL10
      • Increase CD8 cells
    • In Tuberculoid leprosy
      • active cell mediated immune response
        • injures cutaneous nerves
        • including axons, schwann cells & myelin
      • Increase Th1 cytokines: IL2, IFNγ, TNFβ
      • Histology:
        • granulomatous inflammation, scanty bacilli
  • Clinical features
    • Pain fibres affected
      • loss of sensation

Traumatic neuroma

  • Non-neoplastic
  • Occurs at proximal end of severed nerve
    • trauma
    • surgery
  • Clinical features
    • Firm nodule, painful or tender
      • Reactive proliferation of schwann cells, axons & fibrous cells

Tumours of peripheral nerves




  • Cutaneous/ in Peripheral nerve
  • Plexiform type
    • only seen in Neurofibromatosis Type1 (NF1)
  • Tumours in NF1 are more likely to become malignant
    • Malignant tumours are called
      • Malignant Peripheral Nerve Sheath tumours (MPNST)
  • Histology
    • Spindle shaped cells
    • Serpentine nuclei
    • Schwann cells, axons, fibroblastic cells and perineurial cells are present




  • Arise from Schwann cells
  • Histology
    • True encapsulation
    • Antoni type A & Antoni type B areas
    • Verocay bodies
  • Multiple tumours seen in NF2
    • Benign
  • Malignant counterpart is MPNST

Leprosy & Poliomyelitis

  • Definition
    • A chronic bacterial disease of the skin, peripheral nerves and the upper airway
  • One of the most feared diseases
  • Causal organism
    • M. Leprae
  • Early stage
    • painless depigmented patch

Differential diagnosis

  • Tinea vesicolor
  • Pityriasis rosea
  • Birth mark depigmentation
  • Granuloma multiforme
  • Psoriasis
  • Contact dermatitis
  • Avitaminosis B
  • Neurofibromatosis
  • Scleroderma
  • Xathomatosis



  • Infectious agent:
    • Mycobacterium leprae
      • acid fast bacilli
      • cannot grow in bacterial media/culture
      • Grow on
        • mouse foot pads
        • in nine banded armadillo
  • Occurrence
    • World prevalence 10-12 million
    • Prevalence rates >5 per/1000 rural tropics and subtropics
  • Endemic areas
    • SE Asia
    • South Asia
    • Philippines
    • Indonesia
    • India
    • Bangladesh
    • Pacific Islands
    • Tropical Africa
    • Latin America
  • Reservoir
    • Man is the only reservoir of proven significance
    • Feral Armadillos in Louisiana & Texas are affected
    • Naturally acquired leprosy Manageby monkey & chimpanzee
      • captured in  Nigeria and Sierra Leone\

Mycobacterium leprae

  • General
    • Acid fast
      • occurs in intracellular and extracellular
    • Occurs in clumps or bundles
      • globi
    • Affinity for
      • Schwann cells
      • cells of the reticulo- endothelial system
    • They remain dormant in various sites
      • can cause relapse
    • Leprosy is highly infectious disease
      • but low pathogenecity
  • Mode of transmission
    • Contact
      • not clearly established
        • Household
        • prolonged close contact
    • Droplet infection
      • Millions of bacilli are liberated daily
        • in the nasal discharge
          • remain viable for 7days in dried nasal secretions
        • Cutaneous ulcers also shed large amounts of bacilli
  • Incubation Period
    • 9 months – 20 years
      • average 4 years for tuberculoid
      • 3-5  years for lepromatous
    • Disease seen children <3 years
      • 50 cases so far
      • youngest: 2 1/2 month
  • Period of communicability
    • Infectivity is lost in most instances (continuous & regular treatment)
      • within 3 months
        • with Dapsone (DDS) or clofazimine
      • within three days
        • with rifampine
  • Susceptibility and resistance
    • Persistence and form of leprosy depend upon ability to develop cell mediated immunity
  • Lepromin test
    • Intradermal injection of autoclaved M.  Leprae & the presence or absence of induration at 28 days is called Mitsuda reaction
    • Reaction
      • lepromatous leprosy
        • -ve immune reaction
        • Mitsuda reaction
      • tuberculoid disease
        • +ve immune reaction
    • The test gives prognostic information but it is not diagnostic


Intermediate lesion

  • Small macules
    • irregular
    • raised edge
    • pale skin lesions
    • anywhere on the body
      • Most common on
        • back
        • forearm
        • thighs
        • face
  • No sensory loss
  • Normal sweating
  • Pathology –non specific inflammatory reaction
  • 90% spontaneous recovery
    • may progress to any of the three later types
    • depending on the cell-mediated response
      • Tuberculoid leprosy
      • Lepromatous leprosy
      • Borderline leprosy


Tuberculoid leprosy


  • Clinical features
    • One or more sensationless  asymmetrical macules with raised edges
      • In dark skins macules: depigmented
      • in pale skins macules: reddish
    • Affected nerves are thickened
      • ulnar
      • median
      • superficial radial
    • Loss of sweat
    • Loss of sensation
    • Wasting of muscles
  • Skin smear
    • -ve for M. leprae
  • Biopsy shows
    • epithelial granuloma with giant lymphocytes
    • scanty bacilli

Lepromatous leprosy


  • Clinical features
    • Numerous symmetrical distributed, macular, plaque form/nodular skin lesions
      • Leonine facies
        • lion face
      • Skin thickened by infiltration
      • Swelling of nose, ear and lips
    • Proliferation of infection in mucous membranes
      • causes nasal congestion & keratitis
      • Nasal discharge, painful eyes
    • Peripheral neuritis
      • complicated by neuropathies ulcers on limbs
      • lead to disfiguration and disability
    • Loss of sensation, pain and temperature
    • Neuropathic ulcers on
      • hands, feet
      • with loss of fingers and toes
    • Painless burns or ulcers
      • Secondary infection
    • Facial nerve palsy
    • Testis & lymph nodes may be damaged
    • Generalized systemic symptoms
      • fever
  • Skin smear highly +ve for bacilli
  • Immune response highly -ve (Mitsuda reaction)

Borderline leprosy


  • between tuberculoid & lepromatous
  • Mixed clinical features
    • Skin lesions often raised ring shaped lesions
      • with normal or slightly reduced sensation
    • Peripheral nerves may be thickened


Clinical manifestations

  • Signs of peripheral nerves involvement
    • Skin lesions
      • Test for light touch, pin prick & temperature discrimination
      • Hyperesthesia & anesthesia
    • Peripheral nerves
      • Bilateral palpation of peripheral nerves for enlargement and tenderness
        • ulnar at elbow
        • peroneal nerve at head of fibula
        • great auricular nerve
    • Muscles
      • Paralysis
      • muscle wasting
    • Trophic ulcers


  • Clinical examination
    • Examination of
      • skin
      • nerves
      • pain sensation
      • sweating
      • motor functions
      • nerve thickening
  • Laboratory Examination
    • Skin slit smears
      • Skin is slit without drawing blood
      • smear taken & stained for bacilli
        • usually from ear lobes
      • The quantity and the morphology is measured
    • Skin biopsy
      • of lesion edge/nerve
    • Mitsuda reaction (Not diagnostic)
      • Skin test with lepromin
        • made from autocalved Mycobacterium leprae
      • Granulomatous nodule after 28 days in tuberculoid and some boderline cases
      • Healthy persons may show a positive Mitsuda reaction
      • If no reaction –> lepromatous leprosy


Multidrug therapy (MDT)

  • Combinations of
    • Rifampicin
      • urine slightly reddish for few hours
    • Clofazimine
      • brownish black discoloration
      • drness of skin
    • Dapsone
      • allergic reaction towards sulpha drugs
        • itchy skin rashes
        • exfoliative dermatitis
      • do not give to patients who are allergic
  • May develop drug resistance if only 1 drug used


Reactions in leprosy

Non-Lepromatous lepra reaction (Type 1 lepra reaction)

  • Seen following treatment of boderline leprosy
    • Type 4 delayed hypersensitivity reaction
  • Last for few days to several weeks
  • Reactions
    • Acute inflammation of preexisting borderline lesion
    • Skin lesions become swollen and erythematous
    • Neurological lesions
      • ulnar nerve palsy may occur abruptly
    • Both upgrading or reversabile reaction
      • more tuberculoid or more lepromatous

Erythema Nodosum Leprosum (Type 2 lepra reaction)

    • Humeral antibody response to antigen antibody complex
      • type III hypersensitivity reaction
    • systemic manifestations
      • Fever
    • Athralgia
    • Painful subcutaneous erythematous nodules
    • Iritis


Prevention & control of leprosy

  • Primary prevention
    • Health promotion
    • improve housing standards
    • standard of living
    • BCG (Limited protection)
  • Secondary prevention
    • Early diagnosis & treatment
    • WHO-Multi drug treatment
      • follow up 5 years,
      • Tuberculoid – 6 months
      • Borderline & lepromatous – 2 years
  • Tertiary prevention
    • Disability limitation
    • Care of the hands, feet, neuropathy and loss of sight
    • Rehabilitation
      • Restoration of function
      • Deformities, loss of limbs fingers, nose etc





  • Definition
    • An acute viral infection
      • with severity ranging from inapparent infection to non-specific febrile illness, aseptic meningitis, paralytic disease and death
    • Minor illness includes (if the disease progresses)
      • fever
      • malaise
      • headache
      • nausea
      • vomiting
    • Severe illness includes
      • muscle pain
      • stiffness of neck
      • stiffness back with/without paralysis
    • The site of paralysis depends upon the location of the nerve cell destruction in the spinal cord/the brain stem
  • Infectious agent
    • Polio virus Type 1
      • Brunhilde
      • most commonly seen in epidemics
    • Type 2
      • Leon
    • Type 3
      • Lansing (genus Enterovirus)


  • Occurrence
    • Worldwide
    • disease of children & adolescents
  • Reservoir
    • Man only
      • people with inapparent infections
  • Mode of transmission
    • Direct contact through close association
    • Rare instances – fecaloral route
  • Incubation period
    • 7-14 days of paralytic cases
    • Range 3-35 days

Susceptibility and resistance

  • Susceptibility to infection is general
  • paralytic infections are rare
  • Lifelong specific immunity
  • immunisation at birth
  • Infants born to immune mothers have transient passive immunity Injections of other vaccines may provoke paralysis
  • Second attacks are rare
    • due to different type of polio virus
  • Tonsillectomy increases the risk of bulbar involvement
  • Strenuous exercise is known to make the paralysis worse in the exercised limb
  • during the prodromal phase
  • Statistics
    • 90% have no or almost no symptoms/indistinguishable from influenza
    • 9% have non-paralytic polio
    • 1% have spinal/bulbar polio
      • 10% die
      • 50% recover fully
      • 40% are left with only partial recovery/permanent paralysis
    • 0.4% of permanent paralysis,
      • 1 or both lower limbs
    • 0.01%
      • Quadriplegia
      • respiratory paralysis

    Pathophysiology of polio

    • Polio is generalized infection
      • which may involve the whole body including muscles, liver spleen, and gastrointestinal system
    • Anterior horn cells are chiefly affected
      • Degeneration & loss of Nissls granules
        • uptil complete disappearance of the cells
      • This results in the lower motor neuron paralysis
        • with asymmetrical paralysis & normal sensation
        • Paralysis occurs in small proportion & may be minimal to severe
        • Paralysis may cause shortening & decrease diameter of the bones
      • Most common muscles involved
        • extensor of hips
        • extensor of knees
        • dorsiflesion of ankles
        • deltoid
        • triceps
        • thenar muscles
        • respiratory muscles
        • spinal muscles
    • Bulbar paralysis
      • Pharyngeal paralysis
        • inability to swallow food, drinks and own secretions
        • inability to cough and difficulty in speaking
    • Respiratory paralysis
      • Respiratory muscles rare
      • Intercostal muscles
        • Anterior horn cells of the thoracic region
      • Diaphragm
        • Anterior horn cells of mid cervical
    • Fibrillations of muscles
      • Paralyzed muscles show fine ripples of contractions

    Diagnosis of polio

    • Clinical examination
      • confirmation of sudden onset of acute flaccid paralysis (AFP)
        • with no loss of sensation
    • Laboratory culture (stool)
      • isolate virus
        • 100% isolation of virus within 2 weeks of onset
          • WHO criteria for certification of polio free
        • 50% within three weeks of onset
        • 25% within 6 weeks

    Prevention of polio

    • Primary prevention
      • Health education
      • Oral polio virus vaccine (OPV)
        • Live attenuated Sabin Vaccine
        • OPV given in Malaysia in
          • 2nd month
          • 3rd month
          • 5th month
        • Booster
          • 18 months
          • standard 1
      • Intramuscular injection
        • Salk Vaccine
    • Secondary Prevention
      • Early diagnosis and prevention
        • Spinal polio and bulbar polio
      • Disability limitation
        • avoid factors that potentiate paralysis
        • eg. operations, injections & strenuous exercise
      • Prevention of deformities & contractures (of bone?)
    • Tertiary prevention (Rehabilitation)
      • Surgery on contractures
      • equinus foot
      • wheel chair for the disabled

    Eradication of polio

    • Polio transmission is now  limited to about 9 countries
      • Afghanistan
      • Pakistan
      • India
      • Angola
      • Congo
      • Nigeria
      • Somalia
      • Ethiopia
      • Sudan
    • Eradication is possible because the virus affects only humans
      • no animal reservoir
      • no long term carriers
      • virus cannot survive outside the human body for long
    • Acute flaccid paralysis (AFP) is being carried out all countries that have declared free of polio
    • Malaysia is free of polio