The article '02 - Leprosy - Why It Affects People?' provides an overview of the population's distribution and a few determinants of leprosy disease. Here we restrict to only the host and environment-related factors. Agent 'M. leprae' factors are dealt with in separate blogs.
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Leprosy - Epidemiology Insights
The epidemiology of any disease so is of leprosy consists of three factors:
- Host factors
- Agent factors
- Environment factors
It is popularly known as the 'Epidemiologic triad'.
What Host Factors Predispose Leprosy Occurrence?
Various factors in the host are favourable for the leprosy bacteria to grow and manifest into a disease:
Age
- No age is immune to the occurrence of leprosy infection or the disease.
- The disease is usually seen in the age group of 20 to 30 years in highly prevalent areas.
- Contrary to the belief that leprosy is rare or non-existent in young age groups, Brubaker et al. reported 91 cases below one year (1). The youngest child's leprosy case was 3 weeks old from Martinique island near West Indies (2).
- A high proportion of child leprosy cases indicate active transmission of leprosy in the defined geography.
- Leprosy is seen in older age groups in low leprosy prevalent areas.
- Leprosy infection is usually acquired in childhood in high-endemic areas.
Sex
- Leprosy is seen in both genders.
- Both incidence and prevalence of leprosy in adults are seen higher among males, with male to female ratio of 2:1 in most countries (3).
- Gender difference appears relatively more among lepromatous leprosy than among non-lepromatous leprosy cases.
- Leprosy appears to be more common among boys than girls (4), possibly due to neglect of girl child health, greater mobility of male children in the community and related wider exposure (5).
Migration
- Leprosy was considered a rural problem in India. However, increased migration from rural areas to urban areas, poor living conditions like overcrowding, poor ventilation, poor natural lighting, unhealthy nutrition, and environmental conditions favour increased leprosy transmission in urban areas.
- Most leprosy-affected people among migrants require multibacillary treatment. Lepromatous leprosy is reported to be high among migrants (6)
Immunity
- Only a few exposed to leprosy bacteria develop the disease. 95% of the general population is reported to have natural immunity against leprosy.
- Subclinical infections are common in leprosy (7) and may contribute to active immunity.
- Leprosy probably first appears in the indeterminate form at the beginning, which may either heal itself or may evolve in other forms of leprosy like - localized Tuberculoid tuberculoid (TT), disseminated form Lepromatous leprosy (LL), or mid-borderline forms - Borderline Tuberculoid (BT), Borderline borderline (BB), or Borderline lepromatous (BL) (8).
- Lesions may spontaneously heal in about 75% of the affected people, especially those with indeterminate or tuberculoid leprosy. Disease regression is reported to be a pervasive feature among tuberculoid leprosy patients, the mean inactivation rate being 10.9% per year, uninfluenced by age or gender (Noordeen, 1975).
- Reduced cell-mediated immunity (CMI) leads to higher-end leprosy cases, like lepromatous leprosy.
Genetic factors
- The Human Leukocyte Antigen (HLA) system and non-HLA genes affect the individual's susceptibility to leprosy and the manifestation of different types of leprosy (9).
What Environmental Factors Predispose Leprosy Occurrence?
Environment plays a critical role in the transmission of leprosy infection.
- Any untreated leprosy case can spread the infection to the contacts through aerosols released during sneezing, coughing, or conversations.
- The leprosy bacteria are found in the nasal mucosa and nasal discharge and on the skin of the leprosy cases not taking treatment. Nasal secretions of a lepromatous leprosy patient may yield as high as 10 million viable leprosy bacteria per day (10).
- The contacts of the untreated leprosy case may show the presence of M. leprae on their skin, in nasal mucosa or in nasal discharge, which may disappear after initiating treatment of the index leprosy case (11).
- A case-control study reported a significant relationship between environmental hygiene with leprosy incidence and room temperature & leprosy.
- A leprosy bacteria can survive atleast 46 days in moist soil and for 60 days at room temperature (12). Another research reported that M. leprae could remain viable for atleast 8 months in free-living amoebae and amoebic cysts (13).
- The household contacts of an active leprosy case may have nine times greater risk of developing leprosy (14).
References:
1. Brubaker ML, Meyers WM, Bourland J. Leprosy in children one year of age and under. Int J Lepr Other Mycobact Dis. 1985 Dec;53(4):517-23. PMID: 4086915.
2. Montestruc E, Berdonneau R. 2 new cases of leprosy in infants in martinique Bull Soc Pathol Exot Filiales. 1954;47:781–3
3. Kumar R, Singhasivanon P, Sherchand JB, Mahaisavariya P, Kaewkungwal J, Peerapakorn S, Mahotarn K. Gender difference in socio-epidemiological factors for leprosy in the most hyper-endemic district of Nepal. Nepal Med Coll J. 2004 Dec;6(2):98-105. PMID: 16295738.
4. Sehgal VN, Rege VL, Mascarenhas MF, Reys M. The prevalence and pattern of leprosy in a school survey. Int J Lepr Other Mycobact Dis. 1977 Oct-Dec;45(4):360-3. PMID: 564883.
5. Narang, Tarun; Kumar, Bhushan1,. Leprosy in Children. Indian Journal of Paediatric Dermatology: Jan–Mar 2019 - Volume 20 - Issue 1 - p 12-24
doi: 10.4103/ijpd.IJPD_108_18
6. George N, Majeed AP, Sasidharanpillai S, Jishna P, Chathoth AT, Devi K. Clinical profile of leprosy among domestic and migrant patients diagnosed at a tertiary referral centre in North Kerala: A ten-year retrospective data analysis. Indian J Dermatol Venereol Leprol 2022;88:422-5.
7. Barreto, Josafá Gonçalves et al. High rates of undiagnosed leprosy and subclinical infection amongst school children in the Amazon Region. Memórias do Instituto Oswaldo Cruz [online]. 2012, v. 107, suppl 1 [Accessed 6 December 2022], pp. 60-67. Available from: <https://doi.org/10.1590/S0074-02762012000900011>. Epub 17 Dec 2012. ISSN 1678-8060. https://doi.org/10.1590/S0074-02762012000900011.
8. Ridley DS. Classification of leprosy according to immunity. A five-group system. Int J Lepr (1966) 34:255–73.
9. Corrêa Rda G, de Aquino DM, Caldas Ade J, Serra Hde O, Silva FF, Ferreira Mde J, Santos EJ, Mesquita ER. Association analysis of human leukocyte antigen class II (DRB1) alleles with leprosy in individuals from São LuÃs, state of Maranhão, Brazil. Mem Inst Oswaldo Cruz. 2012 Dec;107 Suppl 1:150-5. doi: 10.1590/s0074-02762012000900022. PMID: 23283466.
10. Davey TF, Rees RJW. The nasal discharge in leprosy: clinical and bacteriological aspects. Leprosy Review. 1974;45(2):121–134.
11. Job CK, Jayakumar J, Kearney M, Gillis TP. Transmission of leprosy: a study of skin and nasal secretions of household contacts of leprosy patients using PCR. Am J Trop Med Hyg. 2008 Mar;78(3):518-21. PMID: 18337353.
12. Desikan KV, Sreevatsa. Extended studies on the viability of Mycobacterium leprae outside the human body. Lepr Rev. 1995 Dec;66(4):287-95. PMID: 8637382.
13. Wheat WH, Casali AL, Thomas V, Spencer JS, Lahiri R, Williams DL, McDonnell GE, Gonzalez-Juarrero M, Brennan PJ, Jackson M. Long-term survival and virulence of Mycobacterium leprae in amoebal cysts. PLoS Negl Trop Dis. 2014 Dec 18;8(12):e3405. doi: 10.1371/journal.pntd.0003405. PMID: 25521850; PMCID: PMC4270725.
14. Oliveira MB, Diniz LM. Leprosy among children under 15 years of age: literature review. An Bras Dermatol. 2016 Apr;91(2):196-203. doi: 10.1590/abd1806-4841.20163661. PMID: 27192519; PMCID: PMC4861567.
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