Moraxella catarrhalis: Difference between revisions

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==Classification==
==Classification==


Bacteria; Pseudomonadota; Gammaproteobacteria; Pseudomonadales; Moraxellaceae.
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Gammaproteobacteria
Order: Pseudomonadales
Family: Moraxellaceae
Genus: Moraxella
Species: M. catarrhalis


==Species==
''Moraxella catarrhalis''
{{Uncurated}}[[Image:https://images.fineartamerica.com/images-medium-large-5/moraxella-catarrhalis-dennis-kunkel-microscopyscience-photo-library.jpg|thumb|300px|right|Legend.Image credit: D. Kunkel, Science Photo Library]]


==Description and Significance==
==Description and Significance==
The gram-negative, aerobic diplococcus ''Moraxella (Branhamella) catarrhalis'', formerly known as ''Neisseria catarrhalis'' or ''Micrococcus catarrhalis'', is frequently encountered as a pathogen of the upper respiratory tract (Verduin et al., 2002). Since its discovery in 1896, the bacterium has developed into a true pathogen and is now recognized as a significant contributor of upper respiratory tract infections in some of the more healthy young and senior citizens (Constantinescu, 2021).  
''Moraxella catarrhalis'' is known to cause otitis media, which is inflammation of the inner ear. This is most frequently seen in children and older adults; it does not infect middle-age adults nearly as much. Currently there is no licensed vaccine available for ''M. catarrhalis'', but this is an area of active research due to the high prevalence of pathogenesis and colonization.  
 
''M. catarrhalis'' is also a significant contributor to lower respiratory tract infections, especially in individuals with chronic obstructive pulmonary disease (COPD). It is a major contributor to acute exacerbations of chronic obstructive pulmonary disease (COPD), acute bacterial rhinosinusitis, and strep throat in children (Murphy et al., 2005).
 
==Genome Structure==
1,863,286 nucleotides make up the 1,886 protein-coding genes in the RH4 genome. The genomes of the ATCC 43617 and RH4 strains are comparable, demonstrating the high degree of gene conservation between them. The 16S rRNA and multilocus sequence typing in silico phylogenetic analyses demonstrate that RH4 is a member of the phylogenetic lineage of the ''Moraxella catarrhalis''.
 
Since the genes encoding the enzymes needed for various pathways, cycles, and acetate metabolism are present, RH4 depends on fatty acid and acetate metabolism. The routes for acquiring iron, nitrogen metabolism, and oxidative stress responses are some of the pathways crucial for survival under difficult conditions. The ATCC 43617 strain is categorized as a 16S rRNA type 1 strain, just like RH4 and RH4's genome has a 41.7% GC content (Vries et al., 2010).


==Cell Structure, Metabolism and Life Cycle==
The inferred metabolism of ''Moraxella catarrhalis'' has an uncommon characteristic in that it appears incapable of using any exogenous carbohydrates. The absence of entire glycolytic pathways, all carbohydrate catabolic enzymes, and all carbohydrate transport systems in this bacterium shows ''Moraxella catarrhalis'' does not consume any of the carbohydrate types and does not create acid from glucose. Gluconeogenesis is necessary since exogenous carbohydrates cannot be used. The entire set of enzymes needed for aerobic metabolism is present in ''Moraxella catarrhalis''. The ATP synthase, glyoxylate cycle, electron transport system, and citric acid cycle are all present and functional in this bacteria.


The way ''M. catarrhalis'' uses acetate is associated with a working glyoxylate cycle. In an environment with low-oxygen or a microaerophilic environment nitrate reductase is present, which is compatible with the reported use of nitrate by ''M. catarrhalis''. There are some peculiar features of nitrogen metabolism, such as the fact that ''M. catarrhalis'' appears to contain both glutamate dehydrogenase and glutamate synthase-glutamine synthase routes for ammonia absorption. ''M. catarrhalis'' has the genes for these enzymes, although it is unclear if it can assimilate ammonia. It lacks all regulators linked to nitrogen limitation in organisms like Escherichia coli. High levels of ammonia cannot be assimilated by ''M. catarrhalis''. Although the genes for ammonia assimilation enzymes are present, it is unclear whether they actually work. They might only be used to synthesize glutamate and glutamine, and they might not be sufficiently expressed to take part in the digestion of ammonia. All amino acids, with the exception of proline and arginine, are synthesized by ''M. catarrhalis'' through complete pathways (Wang., 2007).
Characteristics:
* non-motile
* gram-positive
* diplococcus
* aerobic
* oxidase-positive
* sticks to host cell using a trimeric autotransported adhesion (TAA)
* commonly resistant to penicillin, ampicillin, and amoxicillin


==Ecology and Environment==
==Structure, Metabolism, and Life Cycle==
''M. catarrhalis'' displays an endotoxin that is similar to many found in the Neisseria species, which play a role in the disease process. Some strains of ''M. catarrhalis'' exhibit fimbriae or pili, which help the cells adhere to the respiratory epithelium. Also, the cells express specific proteins that allow uptake for iron which act as receptors. ''M. Catarrhalis'' forms round opaque colonies on blood and chocolate agar, and the colonies can be slid around agar surfaces without being disrupted; this is called the "hockey puck sign". One interesting feature of the cellular structure of ''M. catarrhalis'' is the presence of trimeric autotransporter adhesins, which are essentially a type of virulence factor. These are structures of gram-negative bacteria that allow the cells to infect a host through a process called cell adhesion. Another term for trimeric autotransporter adhesins is oligomeric coiled-coil adhesins (OCAs).


''M. catarrhalis'' relies on acetate, lactate, and fatty acids for growth, and it is considered an arginine auxotroph. Adults with illnesses or an autoimmune disease typically carry ''M. catarrhalis'' in their respiratory passages (Simmons et al., 2012). It binds to the host cell through a trimeric autotransported adhesion and is non-motile.  
==Ecology and Pathogenesis==
''Moraxella catarrhalis'' is specifically a human pathogen and it can cause infection in immunocompromised hosts, such as HIV/AIDS patients. Also, it can colonize the upper respiratory tract in children and infants more easily than adults and cause pneumonia and sinusitis. ''Moraxella catarrhalis'' enters the nasopharynx and can invade numerous cell types, including bronchial epithelium, small airway epithelium, and type II alveolar pneumocytes[[#References | [4]]]. It can migrate to the middle ear after it enters the nasopharnyx. It forms a biofilm in vitro, but it is not clear what the function of this biofilm is. The patient will experience symptoms of acute sinusitis, urethritis, septiciema, meningitis, maxillary sinusitis, conjunctivitis, and septic arthritis, and exacerbation of chronic obstructive pulmonary disease[[#References | [3]]].


15%–20% of acute otitis otitis media outbreaks are brought on by the human pathogen ''Moraxella catarrhalis'', which is also a major cause of otitis media in newborns and young children. In the US, ''M. catarrhalis'' is thought to be the source of 2-4 million adult cases of chronic obstructive pulmonary disease. ''M. catarrhalis'' may go unnoticed in samples from the human respiratory system because it mimic Neisseria species in culture. Infancy and childhood are when upper respiratory tract colonization is most common, while adulthood is when it declines significantly (Murphy et al., 2009).
The process of infection includes:
# Adhesion to the host epithelium
# Invasion of the host epithelium
# Biofilm formation
# Evasion of the host immune system
# Nutrient acquisition
## ''M. catarrhalis'' can utilize human transferrin, human lactoferrin, and to some extent human hemoglobin as iron sources, which is mediated by many cell surface iron-binding proteins. There are two specific lactoferrin-binding proteins, LbpA and LpbB, two specific transferrin-binding proteins, TbpA and TbpB, hemoglobin utilization protein, mHuA. ''M. catarrhalis relies'' on acetate, lactate, and fatty acids for growth, and it is considered an arginine auxotroph.


==References==
==References==
 
* [1] Bakri F, Brauer AL, Sethi S, Murphy TF. Systemic and mucosal antibody response to Moraxella catarrhalis following exacerbations of chronic obstructive pulmonary disease. J Infect Dis 2002;185:632-40.
De Vries, S. P., van Hijum, S. A., Schueler, W., Riesbeck, K., Hays, J. P., Hermans, P. W., & Bootsma, H. J. (2010). Genome analysis of moraxella catarrhalis strain RH4, a human respiratory tract pathogen. Journal of Bacteriology, 192(14), 3574–3583. https://doi.org/10.1128/jb.00121-10
* [2] Nicotra B, Rivera M, Luman JI, Wallace RJ.Branhamella catarrhalis as a lower respiratory tract pathogen in patients with chronic lung disease. Arch Intern Med1986;146:890-3.
 
* [3] Tolentino LF. Causes of Moraxella catarrhalis pathogenicity: review of literature and hospital epidemiology. Laboratory Medicine 2007;38:420-1.
Michael Constantinescu, M. D. (2021, August 16). Moraxella catarrhalis infection. Background, Pathophysiology and Etiology, Epidemiology. Retrieved November 16, 2022, from https://emedicine.medscape.com/article/222320-overview#:~:text=Moraxella%20catarrhalis%20is%20a%20gram,Branhamella%20of%20the%20genus%20Moraxella.
* [4] Dirk Linke, Tanja Riess, Ingo B. Autenrieth, Andrei Lupas, Volkhard A.J. Kempf, Trimeric autotransporter adhesins: variable structure, common function, Trends in Microbiology, Volume 14, Issue 6, June 2006: 264-270.(http://www.sciencedirect.com/science/article/pii/S0966842X06000977.)
 
Murphy, T. F., Brauer, A. L., Grant, B. J., & Sethi, S. (2005). moraxella catarrhalis in chronic obstructive pulmonary disease. American Journal of Respiratory and Critical Care Medicine, 172(2), 195–199. https://doi.org/10.1164/rccm.200412-1747oc
 
Murphy, T. F., & Parameswaran, G. I. (2009). moraxella catarrhalis,a human respiratory tract pathogen. Clinical Infectious Diseases, 49(1), 124–131. https://doi.org/10.1086/599375
 
Simmons, J., & Gibson, S. (2012). Bacterial and mycotic diseases of nonhuman primates. Nonhuman Primates in Biomedical Research, 105–172. https://doi.org/10.1016/b978-0-12-381366-4.00002-x
 
Verduin, C. M., Hol, C., Fleer André, van Dijk, H., & van Belkum, A. (2002). moraxella catarrhalis : From emerging to established pathogen. Clinical Microbiology Reviews, 15(1), 125–144. https://doi.org/10.1128/cmr.15.1.125-144.2002
 
Wang, W., Reitzer, L., Rasko, D. A., Pearson, M. M., Blick, R. J., Laurence, C., & Hansen, E. J. (2007). Metabolic analysis of moraxella catarrhalis and the effect of selected in vitro growth conditions on global gene expression. Infection and Immunity, 75(10), 4959–4971. https://doi.org/10.1128/iai.00073-07


==Author==
==Author==
Page authored by Student Savannah Brittain at UNC Wilmington.
Page authored by Aaron Yeshe, student of [mailto:helv0010@umn.ed Mandy Brosnahan], Instructor at the University of Minnesota-Twin Cities, MICB 3301/3303: Biology of Microorganisms.


<!--Do not edit or remove this line-->[[Category:Pages edited by students of Mandy Brosnahan at the University of Minnesota-Twin Cities]]
<!--Do not edit or remove this line-->[[Category:Pages edited by students of Mandy Brosnahan at the University of Minnesota-Twin Cities]]

Latest revision as of 22:35, 20 December 2022

This student page has not been curated.

Classification

Kingdom: Bacteria Phylum: Proteobacteria Class: Gammaproteobacteria Order: Pseudomonadales Family: Moraxellaceae Genus: Moraxella Species: M. catarrhalis


Description and Significance

Moraxella catarrhalis is known to cause otitis media, which is inflammation of the inner ear. This is most frequently seen in children and older adults; it does not infect middle-age adults nearly as much. Currently there is no licensed vaccine available for M. catarrhalis, but this is an area of active research due to the high prevalence of pathogenesis and colonization.


Characteristics:

  • non-motile
  • gram-positive
  • diplococcus
  • aerobic
  • oxidase-positive
  • sticks to host cell using a trimeric autotransported adhesion (TAA)
  • commonly resistant to penicillin, ampicillin, and amoxicillin

Structure, Metabolism, and Life Cycle

M. catarrhalis displays an endotoxin that is similar to many found in the Neisseria species, which play a role in the disease process. Some strains of M. catarrhalis exhibit fimbriae or pili, which help the cells adhere to the respiratory epithelium. Also, the cells express specific proteins that allow uptake for iron which act as receptors. M. Catarrhalis forms round opaque colonies on blood and chocolate agar, and the colonies can be slid around agar surfaces without being disrupted; this is called the "hockey puck sign". One interesting feature of the cellular structure of M. catarrhalis is the presence of trimeric autotransporter adhesins, which are essentially a type of virulence factor. These are structures of gram-negative bacteria that allow the cells to infect a host through a process called cell adhesion. Another term for trimeric autotransporter adhesins is oligomeric coiled-coil adhesins (OCAs).

Ecology and Pathogenesis

Moraxella catarrhalis is specifically a human pathogen and it can cause infection in immunocompromised hosts, such as HIV/AIDS patients. Also, it can colonize the upper respiratory tract in children and infants more easily than adults and cause pneumonia and sinusitis. Moraxella catarrhalis enters the nasopharynx and can invade numerous cell types, including bronchial epithelium, small airway epithelium, and type II alveolar pneumocytes [4]. It can migrate to the middle ear after it enters the nasopharnyx. It forms a biofilm in vitro, but it is not clear what the function of this biofilm is. The patient will experience symptoms of acute sinusitis, urethritis, septiciema, meningitis, maxillary sinusitis, conjunctivitis, and septic arthritis, and exacerbation of chronic obstructive pulmonary disease [3].

The process of infection includes:

  1. Adhesion to the host epithelium
  2. Invasion of the host epithelium
  3. Biofilm formation
  4. Evasion of the host immune system
  5. Nutrient acquisition
    1. M. catarrhalis can utilize human transferrin, human lactoferrin, and to some extent human hemoglobin as iron sources, which is mediated by many cell surface iron-binding proteins. There are two specific lactoferrin-binding proteins, LbpA and LpbB, two specific transferrin-binding proteins, TbpA and TbpB, hemoglobin utilization protein, mHuA. M. catarrhalis relies on acetate, lactate, and fatty acids for growth, and it is considered an arginine auxotroph.

References

  • [1] Bakri F, Brauer AL, Sethi S, Murphy TF. Systemic and mucosal antibody response to Moraxella catarrhalis following exacerbations of chronic obstructive pulmonary disease. J Infect Dis 2002;185:632-40.
  • [2] Nicotra B, Rivera M, Luman JI, Wallace RJ.Branhamella catarrhalis as a lower respiratory tract pathogen in patients with chronic lung disease. Arch Intern Med1986;146:890-3.
  • [3] Tolentino LF. Causes of Moraxella catarrhalis pathogenicity: review of literature and hospital epidemiology. Laboratory Medicine 2007;38:420-1.
  • [4] Dirk Linke, Tanja Riess, Ingo B. Autenrieth, Andrei Lupas, Volkhard A.J. Kempf, Trimeric autotransporter adhesins: variable structure, common function, Trends in Microbiology, Volume 14, Issue 6, June 2006: 264-270.(http://www.sciencedirect.com/science/article/pii/S0966842X06000977.)

Author

Page authored by Aaron Yeshe, student of Mandy Brosnahan, Instructor at the University of Minnesota-Twin Cities, MICB 3301/3303: Biology of Microorganisms.

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