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Leprosy: An Introduction (i)

Throughout the centuries, leprosy has been characterized as a disease responsible for serious deformities resulting in stigmatization and psychological and social suffering. Probably one of the first examples of Public Health regarding leprosy can be found on the Leviticus, where priests are taught the first notions of leprosy diagnosis which were the segregation of those suffering such terrible disease (at that time seen as  prescribed environmental infection control strategies). There is also a mention of leprosy in Al-Bukhari’s Muslim Hadith of Prophet Mohammed’s dread of leprosy (“Escape from the leprous the way you escape from a lion”). Since then leprosy is a metaphor for stigma. Even not so long ago, during the boom years of HIV, those afflicted by AIDS were stigmatized as “unclean”, “outcast” or “incurable” and, hence, pejoratively called as the new lepers of our era.

Leprosy is caused by Mycobacterium leprae and Mycobacterium lepromatosis, the former being one of the first, if not the first, micro-organism directly associated with a specific human disease. M. leprae was first discovered by the Norwegian physicist Gerhard Hansen (1841-1912), hence leprosy is also known as Hansen’s Disease.

However, there are still big gaps in the understanding of leprosy, not only at pathological and immunological levels, but also at some points of its epidemiology. So far, and very roughly, we know that infection does not necessarily lead to any symptoms or lesions specific for the disease. Moreover, we assume that M. leprae is not very pathogenic and that most infections do not result in symptoms. Early symptoms can be self-limiting and skin lesions can heal spontaneously.


How is leprosy distributed?

The total number of leprosy patients in the world varies from 10 to 12 million, increasing by about 500k declared cases every year. The last estimate done by the World Health Organization (WHO) distributes the disease in this way:

–        Asia: 62%

–        Africa: 34%

–        South America: 3%

–        Rest of the World: 1%

Leprosy is known to happen at all ages, ranging from early infancy (the youngest case reported was a three-week old baby in Martinique) to old age. Also, although leprosy affects both sexes in most of the World, males a affected more frequently than females, at a ratio of approximately 2:1.

The factors that contribute to this uneven distribution are, generally, climatic conditions, diet, nutrition and socio-economic factors (literacy, caste, etc.)

How is leprosy transmitted?

The exact mechanism of transmission is still unknown to us, but it is widely accepted that the main way of transmission is through the respiratory route, although there are other possibilities such as transmission through insects that cannot be ruled out.

Nowadays it is thought that there are two main portals of entry for M. leprae: the skin and the upper respiratory tract. Which is the main one? It is still unclear, although the entry through the respiratory tract is the most favoured one (this goes against the historically long-held view that the main portal of entry for M. leprae was the skin).

When M. leprae invades the human body, there are two actions that can take place: tuberculoid leprosy (TT) and lepromatous leprosy (LL).

In tuberculoid leprosy, which is the milder form of the disease, the body’s immune cells attempt to seal off the infection from the rest of the body by surrounding the offending pathogen. Because this response occurs in the deeper layers of the skin, the hair follicles, sweat glands and nerves can be destroyed, resulting in the skin being discoloured, dry and lacking of sensitivity. When nerves of the face, arm and legs are involved, they become enlarged and can be easily felt by the doctor. Also, the reduced numbers of bacteria in this type of leprosy leads to it being referred as paucibacillary leprosy (PB) and is the most prevalent one.

In lepromatous leprosy, which is the most contagious form of the disease, the body’s immune system is unable to organize a strong response to the invading organism. Because of this, M. leprae multiplies freely in the skin. This type of leprosy is also known as multibacillary leprosy (MB), because of the presence of large numbers of bacteria. The main feature of this disease is the appearance of large nodules or lesions all over the body, face and mucous membranes. This type of leprosy can lead to blindness, drastic change in voice and mutilation of the nose.

What are the symptoms?

In tuberculoid leprosy, a rash appears, consisting of one or a few flat whitish areas, which will be numb due to the bacteria damaging the underlying nerves.

In lepromatous leprosy, many small bumps or larger raised rashes of variable size and shape will appear on the skin, therefore the numbed areas of the body will be larger than in TT.

The most severe symptoms result from infection of the peripheral nerves, causing the deterioration of a person’s sensitivity to pain and temperature. Repeated damage could eventually lead to loss of fingers and toes, as well as muscle weakness. Skin infection could lead to areas of swelling and lumps, which might result on disfiguring the face.

During the course of untreated or even treated leprosy, the body’s immune response may produce inflammatory reactions, which in turn can produce fever and inflammation of the skin, peripheral nerves, lymph nodes, testes, kidneys, liver and eyes.

And with this I end the first entry on leprosy. On the next few days I will write about the management of leprosy (diagnosis, treatment, etc.) and two more posts to briefly write about leprosy through History and a homage post to one of the most prominent scientists on the leprosy field.

I hope that you enjoyed the reading and that you have a nice day. God bless you.

On the road to….

Hi guys, I’m sorry I haven’t posted anything since the Dengue fever series, but I can assure you that the new series on Leprosy are being drafted. It is a bit hard and very time consuming to come up with anything half-decent with such a little spare time I have. However, I have the first post lined up and it should be out soon.

Just so you know, to follow with the “tropical” diseases series (that also give the name to the blog), I thought that the perfect post after the leprosy should be TB. Merit also goes towards a colleague pharmacist who suggested it to me not so long ago.

However, due to my chaotic (alas, not always) thought process, other ideas pop in and I tend to do research on them in the middle of my work on whatever I’m working at the time. So, for example, the subject of fillariae (Loa loa, Wuchereria bancrofti, Brugia timori, Onchocerca volvulus etc) has always been of great interest to me since I was a student. I had the opportunity to observe some cameroonian inmigrants affected by loiasis and, trust me, that was an experience that I would think twice to have again and, yet, triggered my interest in that terrible disease and other tropical diseases that are too remote, too ignored by most of us.

Have a good day and God bless you.

Oh, and happy New Year!

Clinical management of dengue

Dengue viruses cause symptomatic infections or asymptomatic seroconversions. Symptomatic dengue infection is a systemic and dynamic disease. It has a wide clinical spectrum that includes both severe and non-severe clinical manifestations.

after the incubation period, the illness begins abruptly and, in patients with moderate to severe disease, is followed by three phases: febrile, critical and recovery. Due to its dynamic nature, the severity of the disease will usually only be apparent during the transition of the febrile to afebrile phase (that transition is also known as defervescence), which often coincides with the onset of the critical phase.

For a disease that is complex in its manifestations, management is relatively simple, inexpensive and very effective in saving lives as long as correct and timely interventions are in place. The key to a good clinical outcome is understanding and being alert to the clinical problems that arise during the different phases of the disease, leading to a rational approach in case management.

Triage and management decisions at primary and secondary care levels are critical in determining the clinical outcome of dengue. A well managed front-line response reduces the number of unnecessary hospital admisions and saves the lives of dengue patients. Early notification of dengue cases seen in primary and secondary care is crucial for indentifying outbreaks and initiating an early response.

1. Febrile phase

Patients normally develop an acute febrile phase suddenly, lasting 2-7 days and being often accompanied by facial flushing, skin erythema, generalized body ache, myalgia (muscular pain), arthralgia (joint pain), retro-orbital eye pain (pain behind the eye), photophobia, headache and rubeliform exanthema (widespread rubella-like rash). Some times a sore throat, an injected pharynx, an injected conjunctive, anorexia, nausea and vomiting can also appear.

However, it can be difficult to clinically differentiate dengue from non-dengue febrile diseases in the early febrile phase. A positive tourniquet test in this phase indicates an increased possibility of dengue, although it is not very reliable as a diagnostic tool. Hence, it is crucial at this stage to look for and monitor warning signs and other clinical and haematological parameters, to identify the progression to the critical phase.

Mild haemorrhagic manifestations may be present: nose and gum bleeding, easy bruising and bleeding at venepuncture sites, massive vaginal bleeding in women of child-bearing age and, less commonly, gastrointestinal bleeding may occur.

The earlies abnormality in the full blood count is a progressive decrease in total white cell count, which should alert the doctor to a high probability of dengue.

2. Critical phase.

During the defervescence period, patients without an increase in capillary permeability will improve without going through the critical phase. However, patients with an increase in capillary permeability may manifest with the warning signs (1), mostly as a result of plasma leakage.

These warning signs mark the beginning of the critical phase: these patients become worse around the time of defervescence, where the temperature drops to 37.5-38C or less and remains below this level, usually on days 3-8 of illness. Progressive leukopenia followed by a rapid decrease in platelet count usually precedes plasma leakage (the period of clinically significant plasma leakage usually lasts 24-48 hours); also, an increase of the haematocrit above the baseline may be one of the earliest signs, and precedes changes in the blood pressure and pulse volume.

The severity of plasma leakage (signalled by an increase of the haematocrit) may be reduced by early intravenous fluid therapy. This is the reason why frequent measurements of the haematocrit level are essential to adjust the intravenous fluid therapy and avoid pulmonary oedema or congestive heart failure during both the critical and recovery phases.

If shock occurs when a critical volume of plasma through leakage, it is often preceded by warning signs. With profound and/or prolongued shock, the body temperature may be subnormal and, due to the loss of plasma, metabolic acidosis, progressive organ impairment (hepatitis, encephalitis, myocarditis, etc) and disseminated intravascular coagulation will appear, which can lead to severe haemorrhage causing the haematocrit to decrese in severe shock.

(1) Warning signs of dengue: usually precede the manifestation of shock, towards the end of the febrile phase and may be persistent vomiting and severe abdominal pain; increasing lethargy, weakness, dizziness or postural hypotension will appear during the shock state. Spontaneous mucosal bleeding or bleeding at previous venepuncture sites are important haemorrhagic manifestations. Hepatitis does usually happen along with fluid accumulation (which only will happen/be detected if plasma leakage is significant or after treatment with intravenous fluids).

3. Recovery phase.

As/if the patient survives the 24-48 hour critical phase, a gradual reabsorption of extravascular compartment fluid takes place in the following 48-72 hours. General well-being improves, appetite returns, GI symptoms abate, diuresis ensues and the haemological parameters stabilize.

However, as mentioned before, acute pulmonary oedema and hypervolaemia (only if intravenous fluid therapy has been excessive and/or has been extended into this period) may occur at this stage.


Thank you for your time, I truly hope that you have enjoyed the reading. My next post will be coming some time soon, do you have any suggestions? 

Have a good day and God bless you.

Background information on Dengue fever.

As I was saying before, dengue fever is a mosquito-borne infection that causes a severe flu-like illness and, sometimes, potentially lethal complications such as the Dengue Haemorrhagic Fever (DHF) and the Dengue Shock Syndrome (DSS). It is caused by the dengue virus, a member of the Flaviviridae(1) family, of which there are four different serotypes: Den 1,2,3 and 4.

The World Health Organization (WHO) has estimated that about 1.5 billion people are at risk of acquiring dengue fever and that approximately 50 million infections occur each year. It mainly happens in urban and suburban areas of tropical and subtropical regions of the world, affecting some 100 countries in Africa, Central and South America, Asia, the eastern Mediterranean area and western Pacific. It has also been found in mainland Europe (France and Croatia mainly) and in Madeira (Portugal), although in a much smaller scale. Dengue fever does not occur in the UK but it has been reported in a number of UK travellers returning from endemic areas: in 2011, there were 223 cases reported in England, Wales and Northern Ireland, a high proportion of whom had acquired their infection in India, Thailand and Pakistan (I will provide a link to the epidemiologic data later on).

Classic dengue fever is a severe, flu-like illness that affects infants, young children and adults but it seldom causes death. The clinical features of dengue fever range from non-existent or mild to severe with mild haemorrhage and vary according to the age of the patient.

The dengue virus is transmited by the bite of an infected female Aedes mosquito. Aedes aegypti is most commonly associated with the transmission of the dengue fever although other species such as Aedes albopticus may also transmit dengue fever in certain circumstances.

When the mosquito feeds on the blood of a person infected with dengue, the virus enters and multiplies inside the mosquito and, after 8-10 days, the mosquito can transmit the virus to another person.

There is no vaccine or drug to prevent dengue fever, the only way, at the present time is to avoid mosquito bites. The Aedes mosquito feeds during the day, particularly around dawn and dusk (unlike Anopheles, which usually bites between dusk and dawn). A good repellent containing DEET must be used on exposed skin together with light cover-up clothing. If a sunscreen is also being used, the repellent must be applied after the sunscreen.

In some endemic areas, dengue control programs rely on the elimination of mosquito breeding sites in the community by regular inspections and insecticide spraying, and the education of local residents to regularly empty standing water and keep outside areas free from waste items in which water may collect. Other methods are being studied, such as the use of genetically modified mosquitoes where their life expectancy is being reduced.

There is no specific antiviral treatment for either classical dengue fever or DHF/DSS, and  supportive nursing care and careful management of symptoms are the standard treatment.

If you acquire dengue fever abroad and become ill on your return to the UK, you cannot pass the infection on to anyone else as the Aedes mosquito needed to transmit the dengue virus is not present in the UK since the temperatures are not consistently high enough for it to breed and thrive.

On the next post I will write about the clinical management of the dengue fever. Have a nice day and God bless you.

(1) The Flaviviridae family comprises the genus Flavivirus which contains 65 related species. They are small, enveloped RNA viruses with peplomers comprising a single glycoprotein E. Other structural proteins are designated C (core) and M (membrane-like). The single strand of RNA is infectious: it functions as the sole messenger. Flaviviruses infect a wide range of vertebrates and many are transmitted by arthropods.

Dengue, an introduction.

Dengue is transmitted by the bite of the Aedes mosquito infected with any one of the four dengue viruses. It occurs in tropical and sub-tropical areas of the world. dengue fever is a febrile illness that affects infants, young children and adults.

Symptoms appear 3-14 days after the infective bite and range from a mild fever to incapacitating high fever, with severe headaches, pain behind the eyes, muscles and joints and, sometimes, a rash.

Severe dengue, accompanied by plasma leakage, severe haemorrhages and organ failure, is potentially a lethal complication, affecting both children and adults. Early clinical diagnosis and a careful clinical management by experienced healthcare professionals increase the survival of patients.

There are no specific antiviral medicines for dengue. It is important to maintain hydration. The use of acetyl-salicylic acid or any other NSAIDs is not recommended. 

In the next couple of posts, I will expand on the background information that we have on the dengue and on the clinical management of the dengue disease. Have a nice day and God bless you.