Multibacillary HD (MB leprosy) patients include a subset known to shed as many as tens of millions of viable bacilli per day. (1) This subset consists of persons with active lepromatous (LL) HD who are not receiving anti-microbial protection. When, and only when, a person with sufficient genomic susceptibility to HD bacilli becomes infected with a sufficient dose of viable bacilli, then that person eventually shows physical signs of disease. Prompt detection of physical signs of HD depends on

A)the index of suspicion among health professionals and among the general population,

B)the level of knowledge and clinical excellence among health professionals, and

C)the frequency of examinations in the general population.

Areas with a low index of suspicion will tend to overlook nearly all transient self-healing forms of HD, leaving only MB forms available for detection. Those with frequent (eg., monthly) examinations of the general population will find even transient forms of HD whose incidence rate is a multiple of that for MB forms. (2) The failure to detect these transient forms does not mean that they did not occur.

The probability of developing physical signs in members of a population is directly related to

a) the quantum of viable bacilli available to that population (notional area under the curve of number of viable bacilli shed per unit time plus the accumulated concentration per unit area of viable bacilli surviving in the environment),

b)the frequency of HD-susceptible genomes in that population,

c)the total person-hours of direct or indirect contact between infectious and genomically susceptible individuals, and

d)the duration for which infectious and susceptible individuals meet in poorly ventilated areas.

In areas of low endemicity, especially in affluent areas, all of these are of low absolute magnitude. Therefore it is predicted, and observed, that in such areas even undiagnosed MB HD patients seem incapable of producing physical signs of HD in others. This does not mean that HD is a non-communicable disease, merely that the viable bacilli shed by untreated LL HD patients never fell on metaphorical “fertile soil”. The most “fertile soil” is a person with a genome conferring extreme susceptibility to bilaterally disseminated and highly bacillated forms of HD. Susceptibility may be expressed in terms of the dose of viable bacilli sufficient to infect 50% of a defined population (ID50). In persons with polar LL genomes, this ID50 is likely to be a very small number of viable bacilli.

In excluding information from most high endemic areas, the authors closed their eyes to some of the most important clues about how HD bacilli are transmitted. This is, of course, the prerogative of any authors. However, it does not inspire full confidence in any claims that the authors may make. Further, the authors are not assisted by the inclusion of a degree of inexactitude. For example, in Uele (now in DR Congo) it was not MDT as we know it that replaced dapsone given alone. It was an experimental regimen for MB HD that included daily rifampicin given for six months alongside ethionamide and dapsone given for a year only. (3) Further, the rapid decline of new MB HD cases with prolonged dapsone continued even after the accumulated backlog of cases was cleared (4). However, this rapid decline in MB HD cases was not maintained once prolonged dapsone was replaced by a multiple-drug regimen given for only a year, despite the inclusion of daily rifampicin given for 6 months. Further, the Uele report authors (4) also were at pains to exclude the possibility that undiagnosed MB HD cases remained undetected in the population. They did this by examining over 99% of persons in two settlements with a total population of nearly 20,000 persons. They found not a single person with MB HD. The rapid decline of new MB HD cases detected had occurred during a period of low and stagnating or declining income. (4)

The main fact emerging from this somewhat non-random sample of reports favoured by the authors appears to be that in low endemic areas transmission is rare despite a 31 month delay in detection of multibacillary cases. This is not surprising, given our understanding of the epidemiology of HD as outlined at the start. Unless an infectious patient meets a person with a genome conferring susceptibility, no new cases with physical signs of HD are expected to arise. In areas of low endemicity this happens with exceeding rarity.

References

1. Davey TF, Rees RJ. The nasal dicharge in leprosy: clinical and bacteriological aspects. Lepr Rev. 1974 Jun;45(2):121-34.
2. Wade H, Ledowsky V. The leprosy epidemic at Nauru. Int J Lepr 1952; 20(1): 1-29.
3. Pattyn SR, Groenen G, Janssens TL. Combined regimens of one year duration in the treatment of multibacillary leprosy-II. Lepr Rev ( 1 989) 60, 1 1 8-123
4. Tonglet R, Pattyn SR, Nsansi BN et al. The reduction of the leprosy endemicity in northeastern Zaire 1975/1989 J.Eur J Epidemiol. 1990 Dec;6(4):404-6 reviewed in: 4a. Almeida J. Reducing transmission in poor hyperendemic areas - evidence from Uele (DRC). LML 29 Nov 2019

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