Leptospira noguchii: Difference between revisions
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<i>Leptospira noguchii</i> are Gram-negative spirochete-shaped bacteria (2). <i>L. noguchii</i> is an emerging pathogen that has been linked to the pathogenic disease Leptospirosis, which is known to affect humans and other mammals, most importantly cattle (2). It has been directly linked to an outbreak with reproductive disorders in a Brazilian dairy goat flock in 2022 (3). | <i>Leptospira noguchii</i> are Gram-negative spirochete-shaped bacteria (2). <i>L. noguchii</i> is an emerging pathogen that has been linked to the pathogenic disease Leptospirosis, which is known to affect humans and other mammals, most importantly cattle (2). It has been directly linked to an outbreak with reproductive disorders in a Brazilian dairy goat flock in 2022 (3). | ||
=3. Genome structure= | =3. Genome structure= | ||
The genome size of <i>L. noguchii</i> (Serovar Panama, Strain U73) is 4.7 Mb and has a GC content of 35.5% ( | The genome size of <i>L. noguchii</i> (Serovar Panama, Strain U73) is 4.7 Mb and has a GC content of 35.5% (4). The genome contains 4034 total genes with 3798 coding genes. Genes relevant to virulence factors included lipoprotein and immunoglobulin-like protein genes <i>lipL41</i>, <i>lipL36</i>, <i>lolC/D</i>, and <i>ligA</i> which are shared by <i>L. interrogans</i>. Several antimicrobial resistance genes are identified which includes efflux pumps (<i>mdtA</i>, <i>mdtB</i>, <i>norM</i>) and metal resistance genes (<i>sugE</i>, <i>czcA</i>, <i>czcD</i>). | ||
<i>L. noguchii</i> serotypes were sourced from various wild and domestic animals, such as cattle, and from human patients. Three serotypes were previously established as Bataviae, Australis, and Autumnalis and were confirmed by the sequencing of the rpoB gene ( | <i>L. noguchii</i> serotypes were sourced from various wild and domestic animals, such as cattle, and from human patients. Three serotypes were previously established as Bataviae, Australis, and Autumnalis and were confirmed by the sequencing of the rpoB gene (5). A recent phylogenetic study yielded sequencing results of the secY locus, identifying additional L. noguchii serogroups Panama and Pyrogenes (6). | ||
=4. Cell structure= | =4. Cell structure= | ||
<i>L. noguchii</i> is a spirochete and Gram-negative bacterium, which has a peptidoglycan cell wall surrounded by an outer membrane of lipopolysaccharide (LPS) (2). They tend to range from 0.1 μm by 6 μm to 0.1 μm to 20 μm ( | <i>L. noguchii</i> is a spirochete and Gram-negative bacterium, which has a peptidoglycan cell wall surrounded by an outer membrane of lipopolysaccharide (LPS) (2). They tend to range from 0.1 μm by 6 μm to 0.1 μm to 20 μm (7). Leptospiral species differ from most pathogenic spirochetes, having a more LPS-rich outer layer (8). Lipid A of leptospires is unique in that it contains a phosphorylated and methylated glucosamine disaccharide unit (2). Leptospires have two periplasmic flagella which allow motility, as well as distinct hooked ends identified through electron microscopy (2). | ||
=5. Metabolic processes= | =5. Metabolic processes= | ||
<i>L. noguchii</i> is a chemoorganotrophic organism and obligate aerobe which metabolizes long chain fatty acids as its main carbon source (2). Alcohol and long-chain fatty acids are the primary carbon and energy sources for <i>L. noguchii</i> ( | <i>L. noguchii</i> is a chemoorganotrophic organism and obligate aerobe which metabolizes long chain fatty acids as its main carbon source (2). Alcohol and long-chain fatty acids are the primary carbon and energy sources for <i>L. noguchii</i> (11). Leptospira also produces catalase, oxidase, and peroxidase which are key in metabolizing compounds during oxidative phosphorylation (11). | ||
=6. Ecology= | =6. Ecology= | ||
<i>L. noguchii</i> grows best at 28-30°C (2). In optimal conditions, <i>L. noguchii</i> has a generation time of about 6-16 hours (11). While <i>L. noguchii</i> is mostly found across the United States and Latin America, the complete biogeographic distribution of <i>L. noguchii</i> remains unknown. The microbe is often recovered from wildlife hosts, which act as a reservoir for the microbe (9). Animals can maintain chronic infection caused by <i>L. noguchii</i> and ultimately spread the microbe through their urine (10). After an infected organism urinates, <i>L. noguchii</i> can spread and enter other organisms through open wounds or when the new organism ingests the microbe (10). | |||
=7. Pathology= | =7. Pathology= | ||
<i>L. noguchii</i> is a pathogenic microorganism that causes leptospirosis in various mammalian species. It enters through openings in the skin, either through mucous membranes or abrasions. It then travels through the bloodstream to the urinary system, which it attaches to through the use of proteins such as LigA, LigB, and LipL32 (11). When leptospires in the blood and tissues reach a critical level, lesions and fever appear. Localized ischemia can in severe cases cause pulmonary damage and hemorrhaging, resulting in jaundice. Tissue damage with leptospirosis, though severe, may be reversible and reparable especially in the kidneys and liver (2). The mechanisms of tissue damage are not well understood, in particular the molecular basis for virulence (2). One of the earliest incidences of <i>L. noguchii</i> infection isolated from humans was characterized through the Fort Bragg strain (Serovar Autumnalis) from soldiers in Fort Bragg, North Carolina (12). | |||
=8. Current Research= | =8. Current Research= | ||
It has been recently discovered that bats can be reservoirs of the <i>Leptospira</i> spp. 30% of the highly diversified <i>Leptospira</i> spp. found in bats were <i>L. noguchii</i>; this host-pathogen association reveals the important roles bats can play in the epidemiology, ecology, and evolution of the bacteria (13). Other researchers have found a new molecular mechanism that could better genetically identify different serovar types of <i>L. noguchii</i>. Through whole genome sequencing of different strains of <i>L. noguchii</i>, horizontal gene transfer of the <i>rfb</i> cluster, which contains many LPS biosynthesis-encoding genes, has been shown to be strongly correlated with the serovar designation of <i>L. noguchii</i> (14). | |||
=9. References= | =9. References= | ||
It is required that you add at least five primary research articles (in same format as the sample reference below) that corresponds to the info that you added to this page. | It is required that you add at least five primary research articles (in same format as the sample reference below) that corresponds to the info that you added to this page. | ||
[Sample reference] Faller, A., and Schleifer, K. "Modified Oxidase and Benzidine Tests for Separation of Staphylococci from Micrococci". Journal of Clinical Microbiology. 1981. Volume 13. p. 1031-1035. | [Sample reference] Faller, A., and Schleifer, K. "Modified Oxidase and Benzidine Tests for Separation of Staphylococci from Micrococci". Journal of Clinical Microbiology. 1981. Volume 13. p. 1031-1035. | ||
Revision as of 14:43, 11 December 2023
1. Classification
Higher order taxa
Bacteria; Spirochaetota; Spirochaetia; Leptospirales; Leptospiraceae; Leptospira
2. Description and significance
Leptospira noguchii are Gram-negative spirochete-shaped bacteria (2). L. noguchii is an emerging pathogen that has been linked to the pathogenic disease Leptospirosis, which is known to affect humans and other mammals, most importantly cattle (2). It has been directly linked to an outbreak with reproductive disorders in a Brazilian dairy goat flock in 2022 (3).
3. Genome structure
The genome size of L. noguchii (Serovar Panama, Strain U73) is 4.7 Mb and has a GC content of 35.5% (4). The genome contains 4034 total genes with 3798 coding genes. Genes relevant to virulence factors included lipoprotein and immunoglobulin-like protein genes lipL41, lipL36, lolC/D, and ligA which are shared by L. interrogans. Several antimicrobial resistance genes are identified which includes efflux pumps (mdtA, mdtB, norM) and metal resistance genes (sugE, czcA, czcD). L. noguchii serotypes were sourced from various wild and domestic animals, such as cattle, and from human patients. Three serotypes were previously established as Bataviae, Australis, and Autumnalis and were confirmed by the sequencing of the rpoB gene (5). A recent phylogenetic study yielded sequencing results of the secY locus, identifying additional L. noguchii serogroups Panama and Pyrogenes (6).
4. Cell structure
L. noguchii is a spirochete and Gram-negative bacterium, which has a peptidoglycan cell wall surrounded by an outer membrane of lipopolysaccharide (LPS) (2). They tend to range from 0.1 μm by 6 μm to 0.1 μm to 20 μm (7). Leptospiral species differ from most pathogenic spirochetes, having a more LPS-rich outer layer (8). Lipid A of leptospires is unique in that it contains a phosphorylated and methylated glucosamine disaccharide unit (2). Leptospires have two periplasmic flagella which allow motility, as well as distinct hooked ends identified through electron microscopy (2).
5. Metabolic processes
L. noguchii is a chemoorganotrophic organism and obligate aerobe which metabolizes long chain fatty acids as its main carbon source (2). Alcohol and long-chain fatty acids are the primary carbon and energy sources for L. noguchii (11). Leptospira also produces catalase, oxidase, and peroxidase which are key in metabolizing compounds during oxidative phosphorylation (11).
6. Ecology
L. noguchii grows best at 28-30°C (2). In optimal conditions, L. noguchii has a generation time of about 6-16 hours (11). While L. noguchii is mostly found across the United States and Latin America, the complete biogeographic distribution of L. noguchii remains unknown. The microbe is often recovered from wildlife hosts, which act as a reservoir for the microbe (9). Animals can maintain chronic infection caused by L. noguchii and ultimately spread the microbe through their urine (10). After an infected organism urinates, L. noguchii can spread and enter other organisms through open wounds or when the new organism ingests the microbe (10).
7. Pathology
L. noguchii is a pathogenic microorganism that causes leptospirosis in various mammalian species. It enters through openings in the skin, either through mucous membranes or abrasions. It then travels through the bloodstream to the urinary system, which it attaches to through the use of proteins such as LigA, LigB, and LipL32 (11). When leptospires in the blood and tissues reach a critical level, lesions and fever appear. Localized ischemia can in severe cases cause pulmonary damage and hemorrhaging, resulting in jaundice. Tissue damage with leptospirosis, though severe, may be reversible and reparable especially in the kidneys and liver (2). The mechanisms of tissue damage are not well understood, in particular the molecular basis for virulence (2). One of the earliest incidences of L. noguchii infection isolated from humans was characterized through the Fort Bragg strain (Serovar Autumnalis) from soldiers in Fort Bragg, North Carolina (12).
8. Current Research
It has been recently discovered that bats can be reservoirs of the Leptospira spp. 30% of the highly diversified Leptospira spp. found in bats were L. noguchii; this host-pathogen association reveals the important roles bats can play in the epidemiology, ecology, and evolution of the bacteria (13). Other researchers have found a new molecular mechanism that could better genetically identify different serovar types of L. noguchii. Through whole genome sequencing of different strains of L. noguchii, horizontal gene transfer of the rfb cluster, which contains many LPS biosynthesis-encoding genes, has been shown to be strongly correlated with the serovar designation of L. noguchii (14).
9. References
It is required that you add at least five primary research articles (in same format as the sample reference below) that corresponds to the info that you added to this page. [Sample reference] Faller, A., and Schleifer, K. "Modified Oxidase and Benzidine Tests for Separation of Staphylococci from Micrococci". Journal of Clinical Microbiology. 1981. Volume 13. p. 1031-1035.
