How fast does Mycobacterium leprae multiply?
M. lepraeis gram-positive, acid-fast bacilli of Mycobacterium lepraecomplex, which is comprised of M. leprae andM. lepromatosis. The former of these two multiply slowly compared to the latter, with an estimated 12 to 13 day generation time.
How does Mycobacterium leprae affect the body?
Mycobacterium leprae is the only bacillus known to selectively invade human peripheral nervous tissue, where an inflammatory process leads to nerve compression and ultimately nerve damage. Mycobacterium leprae is the aetiologic agent of leprosy affecting the skin and peripheral nerves.
Is Mycobacterium leprae non pathogenic?
The majority of Mycobacteria are non-pathogenic and non-parasitic. M. leprae is suspected to be found in the soil, but due to the fact that it can not be plated it is hard to conclude that this is the case (17). DNA from M. leprae has been found in several soil samples within areas known to house outbreaks of leprosy.
When was Mycobacterium leprae first identified?
Mycobacterium leprae, the causative agent of leprosy, was discovered by G. H. Armauer Hansen in Norway in 1873, making it the first bacterium to be identified as causing disease in humans [2, 3].
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Is Mycobacterium leprae acid-fast stain?
Introduction. Mycobacterium tuberculosis and Mycobacterium leprae are acid-fast organisms with lipid-rich cell walls that resist decolorization with acidified alcohol after application of a dye with heat.
Is Mycobacterium leprae acid-fast positive or negative?
Mycobacterium leprae is an acid-fast intracellular Gram-positive bacillus, which shows tropism for macrophages and Schwann cells.
Is leprosy an acid-fast bacteria?
Microbiology. M. leprae is an intracellular, pleomorphic, acid-fast, pathogenic bacterium.
What is an acid-fast organism?
Acid-fast bacteria, also known as acid-fast bacilli or simply AFB, are a group of bacteria sharing the characteristic of acid fastness. Acid fastness is a physical property that gives a bacterium the ability to resist decolorization by acids during staining procedures.
What are examples of acid-fast bacteria?
Bacteria displaying acid fastness include:Genus Mycobacterium – M. leprae, M. tuberculosis, M. smegmatis, M. Avium complex, M. kansasii.Genus Nocardia – N. brasiliensis, N. cyriacigeorgica, N. farcinica, and N. nova.
How can you distinguish Mycobacterium tuberculosis and Mycobacterium leprae?
Major differences among these two bacteria were seen regarding the cell size and thickness of the PG layer. M. leprae had a smaller cell size and a thinner PG layer than M. tuberculosis.
Is Mycobacterium tuberculosis acid-fast?
Sputum, or phlegm, is often used to test for Mycobacterium tuberculosis, to find out if a patient has TB. This bacterium is completely acid-fast, which means the entire cell holds onto the dye.
Is Mycobacterium leprae intracellular?
Mycobacterium leprae, the causative agent of leprosy disease, is a gram-positive bacterium known to live in human and armadillos (Lienhardt et al., 2012). It is an obligate intracellular parasite that cannot grow outside the host cell and not even in the culture medium (Cole et al., 2001).
Why is Mycobacterium leprae difficult to culture?
leprae to rely on the host cell to survive. The bacteria needs an extremely specific environment to thrive in. It is extremely difficult to culture Mycobacterium leprae. All attempts to create a medium that the bacteria are able to grow in has failed.
Which parasite is acid-fast?
Acid fast Intestinal parasites - Parasitology isospora cyclospora - sarcocystis - microsporidium - cryptosporidium - balantidiumt.
What are examples of non acid-fast bacteria?
Some examples of non-acid fast bacteria include:Escherichia coli (Gram-negative bacteria)Bacillus subtilis (Gram-positive bacteria)Salmonella typhi (Gram-negative bacteria)Streptococcus pneumoniae (Gram-positive bacteria)Staphylococcus aureus (Gram-positive bacteria)Pseudomonas aeruginosa (Gram-negative bacteria)
Why is Mycobacterium called acid-fast bacilli?
Mycobacteria are called acid-fast bacilli because they are rod-shaped bacteria (bacilli) that can be seen under the microscope following a staining procedure in which the bacteria retain the color of the stain after an acid wash (acid-fast).
How long does it take for Mycobacterium leprae to grow?
Antibiotic sensitivities are determined through the ability of the organism to grow in mice fed different concentrations of antibiotics. The organism generation time is extremely long, around 14 days on average, thus the determination of antibiotic sensitivity takes several months.
What is the spectrum of Mycobacterium leprae?
Mycobacterium leprae causes granulomatous disease, anesthetic skin lesions, and nerve damage immune reactions. Spectrum of disease runs from tuberculoid leprosy with few bacilli and a granulomatous response to many organisms with little granulomatous response as lepromatous leprosy. The organisms do not grow in culture and are diagnosed by biopsy ...
What is the cause of leprosy?
Mycobacterium leprae causes leprosy—a chronic disease characterized by neuropathies, muscle weakness, and disfigurements. About one-third of people with paucibacillary leprosy have M. leprae positive in saliva by qPCR, 18 as it had been previously suggested by using conventional PCR. 73 Leprosy is transmitted during close and frequent contacts with untreated cases, transmission being mainly via droplets, usually from the nose but also the mouth, but it is not highly infectious. 74 Most people in leprosy-endemic populations have been exposed to M. leprae, yet few develop disease—suggesting that most people develop protective immunity. 75 However, the presence of the M. leprae DNA in buccal swabs of leprosy patients and household contacts indicate an additional strategy for dental clinics. 76
What is the aetiologic agent of leprosy?
Mycobacterium leprae. Mycobacterium leprae is the aetiologic agent of leprosy affecting the skin and peripheral nerves. The infection is currently found in over 100 countries often located in high-burden areas against a low-burden background of cases.
Why is M. leprae considered a metabolic restriction?
The genome of M. leprae predicts severe metabolic restrictions due to a multitude of gene disruptions and deletions. Because of the inability to culture the M. leprae in vitro, animal models continue to provide a basis for testing new drugs and vaccines and offer insight into basic mechanisms of pathogenesis.
How long does it take for a mouse footpad to double?
The organism has a long doubling time of 13 days in the mouse footpad, selectively invades peripheral nerves, and grows preferentially at temperatures of 33–35°C. M. leprae does not produce any known toxins, and tissue injury is caused by the host's immune response or by the sheer mass of infecting bacilli.
When was the genome of M. leprae sequenced?
In 2001, the genome of M. leprae was sequenced. The organism appears to have undergone extensive reductive evolution with considerable downsizing of its genome compared with Mycobacterium tuberculosis. Almost half of the genome is occupied by pseudogenes.
How long does it take for Mycobacterium leprae to double?
Mycobacterium leprae is an acid fast Gram-positive bacterium, with a slow doubling time of 14 days. The slow doubling time is due to the restricted intake of nutrients through the pores in the large waxy walls. Mycobacteria have a unique lipid that makes up their membranes that gives them their unique characteristic.
How does Mycobacterium leprae spread?
Transmission of Mycobacterium leprae is either from infected individual to non-infected individual or from infected individual to environment to non-infected individual (1). Current research suggests that M. leprae that lingers in the environment may be the reason for relapses and epidemics in specific regions.
What is the disease of leprae?
M. leprae is responsible for the disease leprosy (1). In 2006, there were 219,826 cases of leprosy reported. It primarily affects the peripheral nerves and skin (9). It is also known to affect the central nervous system, mucus lining of the mouth, throat and lungs. Patients often experience numbness, skin lesions, joint pain and weakness. Lesions of the skin can leave individuals physically maimed and socially shunned. The innate immune response to the infection is inflammation. The inflammation in the neural cell causes neuropathy and serious nerve damage. Nerve damage doesn't occur until an immune response happens. The nerve damage quickly progresses to numbness, paralysis and deformity (9). Damage due to the immune response of the host also occurs in lung tissue during Mycobacterium tuberculosis infections. Damage of optical nerves can lead to blindness. Leprosy causes blindness in 3.2% of patients, this type of extreme symptoms occurs when treatment isn't sought (1). The treatments for leprosy are multidrug therapy (1). Unlike Mycobacterium tuberculosis, HIV doesn't change the rate of infection or the severity of the infection of M. leprae. Individuals infected with both HIV and leprosy do not see an increased virulence of leprosy or HIV. This is due to leprosy's long incubation times and slow growth rate. The slow growth rate may allow for the host's immune system to fight M. leprae even with an immunodeficiency (9). Two genes have been identified in producing a resistance to M. leprae infections, PARK2/PACRG in humans and NRAMP1 in mice (9).
What is the name of the bacterium that is found in the skin of mice?
Mycobacterium leprae is an intracellular bacterium, infecting nerve, skin and mucosal cells. In laboratory environments, Mycobacterium leprae is cultured on the feet of mice or on nine banded armadillos due to the inability to culture in vitro.
What is the cause of leprosy?
In 2004, The World Health Organization reported that there were 407,791 new cases of leprosy. Leprosy is a serious world issue; in Brazil, India, Democratic of Congo, Tanzania, Nepal, Mozambique, Madagascar, Angola and the Central African Republic leprosy is a major problem. Mycobacterium leprae is an intracellular bacterium, infecting nerve, skin and mucosal cells. In laboratory environments, Mycobacterium leprae is cultured on the feet of mice or on nine banded armadillos due to the inability to culture in vitro.
What temperature is the best temperature for leprosy?
Leprosy is very specified when it comes to infecting hosts. Its ideal conditions are around 33 degrees C , which is lower than most mammals. Mammals with lower temperatures are better hosts for leprosy.
How many people are blind from leprosy?
Leprosy causes blindness in 3.2% of patients, this type of extreme symptoms occurs when treatment isn't sought (1). The treatments for leprosy are multidrug therapy (1). Unlike Mycobacterium tuberculosis, HIV doesn't change the rate of infection or the severity of the infection of M. leprae.
What is the morphology of Mycobacterium leprae?
Mycobacterium leprae is straight rods about 1 – 8 x 0.2 – 0.5µm and it appears either single or groups. It is an intracellular low acid-fast bacillus with 5% H2SO4. It is bound together like cigar bundles by a lipid-like substance called Glia.
When was the Lepra test discovered?
It is a test used for a known prognosis but not a diagnosis. It is discovered by Mitsuda in 1919. It shows the type four hypersensitivity reaction (delayed hypersensitivity reaction) and an intact CMI against the lepra antigen.
How long does a mouse footpad stay in the footpad?
They only cultivate M. leprae is by inoculating the specimens intradermally into footpads and keep in at 20 degrees Celcius for 6-9 months.
How to collect mucus sample in the morning?
In this method, the early morning mucus sample is collected by blowing the patient’s nose on a clean cellophane sheet.
How many samples are there for leprosy?
In the case of leprosy, there is a total of six samples are collected from different places such as four from the skin (forehead, cheek, chin, and buttock), one from the ear lobe, and one from the nasal mucosa by nasal scraping/blow.
Where do mycobacteria go?
Pathogenesis of Mycobacterium leprae. At first, bacilli enter through the respiratory tract and peripheral nerve such as Schwann cells in cooler places (cutaneous nerve and peripheral nerve trunks of limbs and face), and then bacilli multiply in the Schwann cells. After multiplication, they go to either good or weak cell-mediated immune (CMI) ...
Is lepromin positive or negative?
It is positive in tuberculoid patients, negative in lepromatous patients. The positive test is indicated by a nodule formation with more than 5 mm size at the site of inoculation and which ulcerates later on. Uses of Lepromin test. Lepromin test used to classify the lesions of leprosy patients.
How long does it take for leprosy to develop?
On average, the disease incubation period is 5 years but symptoms may occur within 1 year. It can also take as long as 20 years or even more to occur.
When was leprosy first discovered?
Although leprosy was managed differently in the past, the first breakthrough occurred in the 1940s with the development of the medicine dapsone.
What is the WHO recommended treatment for leprosy?
In 2018, WHO reviewed available evidence on key issues related to elimination of leprosy and developed ‘WHO guidelines for the diagnosis, treatment and prevention of leprosy’, recommending a three-drug regimen (rifampicin, dapsone and clofazimine) to both pauci-bacillary and multibacillary types of leprosy.
How many leprosy cases have been treated with MDT?
More than 16 million leprosy patients have been treated with MDT over the past 20 years since its introduction. A general reduction in new cases, though gradual, has been observed in several countries. New cases were reduced to 202 256 in 2019. Many countries reported only a handful of cases, while 45 countries reported zero new autochthonous leprosy cases.
What is the best medicine for pauci-bacillary disease?
In 1981, WHO recommended MDT. The currently recommended MDT regimen consists of three medicines: dapsone, rifampicin and clofazimine. This treatment lasts six months for pauci-bacillary and 12 months for multi-bacillary cases. MDT kills the pathogen and cures the patient.
How much is the reduction in leprosy rate per million children?
90% reduction in rate per million children of new child cases with leprosy
What is the WHO technical guide for leprosy?
In 2020, WHO published the technical guide: a Leprosy/Hansen Disease: M management of reactions and/ prevention of disabilities. This document provides hands-on guidance to health workers to prevent or manage lepra reactions, intermittent and recurring inflammatory episodes that may occur in as many as 50% of cases.
Where does M. leprae exit?
Two exit routes of M. lepraefrom the human body often described are the skin and the nasal mucosa. Lepromatous cases show large numbers of organisms deep in the dermis, but whether they reach the skin surface in sufficient numbers is doubtful [20]. Although there are reports of acid-fast bacilli being found in the desquamating epithelium of the skin, there are reports that no acid-fast bacilli were found in the epidermis, even after examining a very large number of specimens from patients and contacts [21]. However, fairly large numbers of M. lepraewere found in the superficial keratin layer of the skin of lepromatous leprosy patients, suggesting that the organism could exit along with the sebaceous secretions [22]. The quantity of bacilli from nasal mucosal lesions in lepromatous leprosy ranges from 10,000 to 10,000,000 [23]. Majority of lepromatous patients show leprosy bacilli in their nasal secretions as collected through blowing the nose [24]. Nasal secretions from lepromatous patients could yield as much as 10 million viable organisms per day [25].
What is the susceptibility of mycobacteria?
The susceptibility to the mycobacteria and the clinical course of the disease are attributed to the host immune response, which heralds the review of immunopathology of this complex disease. 1. Introduction. Leprosy, also known as Hansen's disease, is a chronic infectious disease caused by Mycobacterium leprae, ...
How many poles of leprosy are there?
Leprosy is classified within two poles of the disease with transition between the clinical forms [42]. Clinical, histopathological, and immunological criteria identify five forms of leprosy: tuberculoid polar leprosy (TT), borderline tuberculoid (BT), midborderline (BB), borderline lepromatous (BL), and lepromatous polar leprosy (LL). Patients were divided into two groups for therapeutic purposes: paucibacillary (TT, BT) and multibacillary (midborderline (BB), BL, LL) [43]. It was recommended later that the classification is to be based on the number of skin lesions, less than or equal to five for paucibacillary (PB) and greater than five for the multibacillary (MB) form.
What are the types of leprosy reactions?
They are classified as type I (reversal reaction; RR) or type II (erythema nodosum leprosum; EN L) reactions. Type I reaction occurs in borderline patients (BT, midborderline and BL) whereas ENL only occurs in BL and LL forms. Reactions are interpreted as a shift in patients' immunologic status. Chemotherapy, pregnancy, concurrent infections, and emotional and physical stress have been identified as predisposing conditions to reactions [51]. Both types of reactions have been found to cause neuritis, representing the primary cause of irreversible deformities.
What is the pathogen of leprosy?
2. Mycobacterium leprae. M . leprae, an acid-fast bacillus is a major human pathogen. In addition to humans, leprosy has been observed in nine-banded armadillo and three species of primates [5]. The bacterium can also be grown in the laboratory by injection into the footpads of mice [6].
What are the genetic factors that influence leprosy?
Human genetic factors influence the acquisition of leprosy and the clinical course of disease [12]. Single-nucleotide polymorphism (SNP) association studies showed a low lymphotoxin-α(LTA)-producing allele as a major genetic risk factor for early onset leprosy [13]. Other SNPs to be associated with disease and/or the development of reactions in several genes, such as vitamin D receptor (VDR), TNF-α, IL-10, IFN-γ, HLA genes, and TLR1 are also suggested [14–17]. Linkage studies have identified polymorphic risk factors in the promoter region shared by two genes: PARK2, coding for an E3-ubiquitin ligase designated Parkin, and PACRG [18]. A study also suggests that NOD2 genetic variants are associated with susceptibility to leprosy and the development of reactions (type I and type II) [19].
What is the disease of leprosy?
Abstract. Leprosy, also known as Hansen's disease, is a chronic infectious disease caused by Mycobacterium leprae, a microorganism that has a predilection for the skin and nerves. The disease is clinically characterized by one or more of the three cardinal signs: hypopigmented or erythematous skin patches with definite loss of sensation, ...
Overview
Microbiology
M. leprae is an intracellular, pleomorphic, acid-fast, pathogenic bacterium. It is an aerobic bacillus (rod-shaped bacterium) with parallel sides and round ends, surrounded by the characteristic waxy coating unique to mycobacteria. In size and shape, it closely resembles Mycobacterium tuberculosis. This bacterium often occurs in large numbers within the lesions of lepromatous leprosy that are usually grouped together like bundles of cigars or arranged in a palisade. Due t…
Microscopy
Optical microscopy shows M. leprae in clumps, rounded masses, or in groups of bacilli side by side, and ranging from 1–8 μm in length and 0.2–0.5 μm in diameter. The organism has been successfully grown on an artificial cell culture medium on a very limited basis by researcher Arvind Dhople. This can be used as a diagnostic test for the presence of bacilli in body lesions of suspected lep…
Pathogenesis
The incubation period of M. leprae can range between 9 months and 20 years. It replicates intracellularly inside histiocytes and nerve cells and has two forms. One form is "tuberculoid," which induces a cell-mediated response that limits its growth. Through this form, M. leprae multiplies at the site of entry, usually the skin, invading and colonizing Schwann cells. The microbe then induces T-helpe…
Genome
Mycobacterium leprae has the longest doubling time (at 13 days of doubling time in the mouse footpad. ) of all known bacteria and has thwarted every effort at culture in the laboratory. Comparing the genome sequence of M. leprae with that of M. tuberculosis provides clear explanations for these properties, and reveals an extreme case of reductive evolution. Less than half of the genome contains functional genes. Gene deletion and decay appear to have eliminate…
Ancient Mycobacterium leprae
Almost complete sequences of M. leprae from medieval skeletons with osteological lesions suggestive of leprosy from different Europe geographic origins were obtained using DNA capture techniques and high-throughput sequencing. Ancient sequences were compared with those of modern strains from biopsies of leprosy patients representing diverse genotypes and geographic origins, giving new insights in the understanding of its evolution and course through history, phyl…
Evolution
The closest relative to M. leprae is M. lepromatosis. These species diverged 13.9 million years ago (95% highest posterior density 8.2 million years ago – 21.4 million years ago ) The most recent common ancestor of the extant M. leprae strains was calculated to have lived 3,607 years ago [95% highest posterior density 2204–5525 years ago]. The estimated substitution rate was 7.67 x 10 …
Symptoms of Mycobacterium leprae
The symptoms of M. leprae, also known as leprosy, are unattractive skin sores that are pale in color, lumps or bumps that do not go away after several weeks or months, nerve damage which can lead to complications with the ability to sense feeling in the arms and legs as well as muscle weakness. Symptoms usually take 3–5 years from being exposed to manifest within the body. Howe…
Classification
Description and Significance
Genome Structure
Cell Structure and Metabolism
- Mycobacterium lepraeis an acid fast Gram-positive bacterium, with a slow doubling time of 14 days. The slow doubling time is due to the restricted intake of nutrients through the pores in the large waxy walls. Mycobacteria have a unique lipid that makes up their membranes that gives them their unique characteristic. The mycolic acids are very large...
Ecology
Pathology
Current Research
References