Members of the group usually appear red or pink on Gram stain. Either the strain or the species of the group has a pili that aids in the adhesion to epithelial cells. One of the unique characteristics of the group is their ability to form biofilms which have a protective mechanism towards other bacteria. Bacterial biofilms are defined as communities of bacteria intimately associated with each other and included within an exopolymer matrix. Biofilms can consist of a single species or multiple species that show commensalism and competitive behavior within the biofilm milieu.
1. The
Neisseria Group
2. The
Branhamella Group
3. The
Veillonella Group
4. The
Megasphaera Group
THE NEISSERIA GROUP
Characteristics:
1. They are gram negative diplococci, kidney or bean shaped with flattened adjacent side. They are aerobic, facultative anaerobes requiring 5 – 10% CO2 for growth.
2. They are oxidase and catalase positive.
3. They are encapsulated, non–motile, non–sporeformers. They ferment a variety of carbohydrates forming acid but not gas.
4. Susceptible to adverse environmental conditions such as drying, chilling, exposure to unfavorable pH or sunlight.
5. Both gonococci and meningococci contain endogenous sialyltransferases.
6. Some members of the group are normal inhabitants of the human respiratory tract and occur extracellularly; others like gonococci and meningococci which are human pathogen occur intracellularly.
7. They have surface proteins, called Opa proteins, that bind to receptors on immune cells and suppress the immune response. As a result, the host is unable to develop immunological memory.
8. Neisseria mainly rely on their ability to utilize host iron–binding proteins transferrin, lactoferrin, and hemoglobin as iron sources. Each iron–binding protein has its own specific receptors on the bacterial cell surface, but they are similar to each other, consisting of a TonB–dependent transporter and a lipoprotein.
Cultural characteristics:
1. They are fastidious organisms requiring enriched media for growth.
2. They form convex, glistening, elevated, mucoid colonies that are transparent, non–hemolytic, non–pigmented.
3. Iron is required for growth. Starch, cholesterol, or albumin is added to neutralize the inhibitory effect of fatty acids present in the medium.
4. They require glucose, pyruvate, or lactate as sole carbon source with a certain level of environmental CO2 tension to initiate growth.
5. They produce grayish white colonies on Thayer–Martin medium. On gram–stained smear, these two pathogenic species are seen intracellularly in leucocytes, signifying their capacity to produce acute infection.
6. Media used:
a. Chocolate Agar Plate (CAP)
b. Thayer Martin medium with VCN (a modified medium of CAP)
V – Vancomycin –
inhibits gram (+) organisms
C – Colistin –
inhibits gram (–) organisms including non–pathogenic Neisseria
N – Nistatin – inhibits fungi
c. Transgrow medium – modification of Thayer–Martin used as transport medium
d. MHA,
Martin–Lewis agar, New York City medium
NEISSERIA MENINGITIDIS / NEISSERIA INTRACELLULARIS
Neisseria meningitidis is a Gram-negative diplococcus pathogen that colonizes the human nasopharynx as a unique host. This organism subsequently spreads into the bloodstream, where it causes septicemia and induces meningitis when it passes through the blood-brain barrier (BBB) and reaches the cerebrospinal fluid (CSF). To reach the bloodstream or CSF, they must adhere to and invade several epithelial and endothelial cells, including the BBB. They ferment glucose in addition to maltose that distinguishes them from Neisseria gonorrhoeae which only ferments glucose.
Carriage of meningococcus in general does not lead to disease. During non-epidemic periods, adults are colonized by meningococcus, this suggests that, like so many other bacterial infections, host rather than bacterial factors determine the outcome. The first and most important line of defense against infection with Neisseria meningitidis and other pathogens is the integrity of the mucosal membrane. People with properdin deficiency are prone to meningococcal infections.
Phenotypic Classification of Neisseria meningitidis:
Four antigenic surface structures can be distinguished on the meningococci: Capsular Polysaccharide (CPS), Outer Membrane Proteins (OMP), Lipopolysaccharide (LPS) and surface appendages known as pili.
1. Serogroups – based on the difference in the structure of Capsular Polysaccharide (CPS). There are 13 serogroups, six of them are the main cause of disease. The capsule is essential for the survival of the organism in the blood as it provides resistance to antibody/complement–mediated killing and inhibits phagocytosis.
a. Serogroup A (MenA) is predominantly found in Africa and Asia – the main meningococcal capsular polysaccharides associated with invasive disease are composed of sialic acid derivatives, Serogroup A capsule consists instead of repeating units of N–acetyl–mannosamine–1–phosphate.
b. Serogroup B (MenB), Serogroup C (MenC), and Serogroup Y (MenY) are most common in North America and Europe – Group B meningococci are relatively resistant to serum bactericidal activity and more susceptible to killing by human neutrophils while Group Y meningococci are relatively susceptible to the bactericidal activity of serum and resistant to killing by neutrophils.
c. Serogroup W135 (MenW) is found in parts of Africa and South America
d. Serogroup X (MenX) is reported in parts of Africa.
2. Serotypes – based on the difference in Class 2/3 Outer Membrane Protein (OMP). These are Types 1, 2a, 2b, 4, 14 and 15.
a. Subserotype – based on the differences in Class 1 outer membrane protein (OMP). These are the Types P1.1, P1.2, P1.4, P1.5, P1.6, P1.7, P1.9, P1.10, P1.12, P1.14, P1.15, P1.16.
3. Immunotypes – based on the difference in oligosaccharide structure of the Lipopolysaccharide (LPS) labeled from L1 to L11. These oligosaccharides are bi– or triantennary structures, which are linked to the KDO (2–keto–3–deoxyoctulosonic acid) molecule.
Structure of Neisseria meningitidis:
1. Capsule – the capsular polysaccharides of the serogroups B, C, W–135 and Y contain sialic acid [NANA (5-N-acetyl-neuramic acid). The incorporation of sialic acids into the capsule and LPS enables bacteria to become less visible to the immune system, as sialic acids are also commonly present on host cell surfaces. The most striking mimicry, however, occurs in serogroup B capsule as this α (2–8)–linked sialic acid homopolymer is structurally identical with a component of human NCAM (neural cell-adhesion molecule), crucial for functional plasticity of the central and peripheral nervous systems. Such identity is responsible for the particularly poor immune response generated against serogroup B capsule by humans. There is a direct correlation between LPS levels and severity of meningococcal disease. LPS also induces the release of chemokines, reactive oxygen species (ROS), and nitric oxide (NO).
Meningococcal LPS consists of three parts:
a. Lipid A – containing hydroxy fatty–acid chains and phosphoethanolamine. Meningococcal lipid A, a disaccharide of pyranasol N–acetyl glucosamine residues, is responsible for much of the biological activity and toxicity of meningococcal endotoxin. Meningococci are resistant to cationic antimicrobial peptides (CAMPs) due to the Lipid A phosphoethanolamine structures present on lipid A head groups. CAMPs are present in macrophages and neutrophils, and occasionally produced by epithelial cells at mucosal surfaces. These peptides play an important role in host defense against microbial infection and are key components of the innate immune responses through their nonoxidative killing action and their signaling functions.
b. Core oligosaccharide containing 2–keto–3–deoxyoctulosonic acid (KDO) – connects Lipid A and the first heptose (α–chain). A second heptose (β-chain heptose) is connected to the first heptose. The variable substitution of the first and second heptose accounts for 11 different immunotypes.
c. Two heptoses (L–glycero–D–manno–heptopyranoside) – the heptose residues provide linkage to the short oligosaccharide residues of the α-, β-, and γ-chains.
Two types of epitopes can be distinguished with meningococcal LPS:
a. Immunotype–specific
epitopes
b. Cross–reactive epitopes
2. Outer Membrane (OM) – a peptidoglycan layer. The structure of peptidoglycan of different strains consists of a maximum of two layers with different variations in the degree of cross–linking and O–acetylation. Typically, the percentage of cross–linking of the meningococcal peptidoglycan is around 40%, like other gram–negative bacteria. The O–acetylation of peptidoglycan results in resistance to lysozyme and to other muramidase. Also, peptidoglycan structures are recognized by components of the innate immune system.
a. The outside layer is composed of lipooligosaccharide (LOS) and proteins. Meningococcal LOS (endotoxin) plays a role in the adherence of the meningococcus and in activation of the innate immune system. They lack the repeating O–side chain of LPS found in enteric gram–negative bacilli. Meningococcal LOS binds to a series of host transfer molecules and receptors on monocytic and dendritic cells of the innate immune system, including LPS-binding protein (LBP), CD14, and myeloid differentiation protein 2 (MD2), part of the Toll-like receptor 4 (TLR4) complex. This triggers the secretion of various cytokines (including IL-6 and TNF-α) that at high levels can result in endothelial damage and capillary leakage.
b. The inside layer is composed of phospholipids that contain proteins primarily responsible for regulating the flow of nutrients and metabolic products. The major phospholipid component of Neisseria membranes consists largely of phosphatidylethanolamine (PE), with varying amounts of phosphatidylglycerol (PG), cardiolipin (CL), and phosphatidate (PA).
Meningococci contain four classes of Outer Membrane Proteins (OMPs), i.e., class 1, 2/3, 4 and 5 proteins which are classified based on their molecular mass.
a. Class 1 has been named PorA which is a cation selective transmembrane protein of 45 KDa that forms trimeric pore in the meningococcal outer membrane. PorA is a major component of OM vesicle-based vaccines and a target for bactericidal antibodies.
b. Class 2/3 has been named PorB which are porins which permit the passage of small hydrophilic solutes across the membrane. It is the major OM porin that inserts in membranes, induces Ca2+ influx and activates Toll– like Receptor 2 (TLR2) and cell apoptosis.
c. Class 4 which is designated as Reduction modifiable protein M (RmpM), because its electrophoretic mobility is influenced by the presence of a reducing agent, may play a role in connecting the outer membrane to the underlying peptidoglycan layer.
d. Class 5 are Opa proteins which play a role in adhesion to, and invasion of host cells. Opa interacts with multiple members of the CEACAM (carcinoembryonic antigen-related cell-adhesion molecule) family; during inflammation high levels of CEACAM are expressed, facilitating Opa interactions and therefore cellular attachment and invasion. Opa proteins are expressed by both meningococci and gonococci.
3. Pili – contributes to the adhesive property of the capsule. It extends several thousand nm beyond the capsule and initiates binding to epithelial cells. Twitching motility generated by pilus retraction is important for passage through the epithelial mucus layer, movement over epithelial surfaces, and microcolony formation. Piliated meningococci attach to human nasopharyngeal cells in greater numbers when compared to meningococci devoid of pili. In addition, pili are involved in facilitating the uptake of DNA by meningococci and enable adherence to endothelial cells and erythrocytes. Neisserial pili can undergo posttranscriptional modifications such as pilin glycosylation. Glycosylation may promote secretion of the soluble pilin units that compete for both anti-pili antibodies and host cell receptors allowing protection of the organism. Meningococci can produce two structurally distinct types of pili–Class I and II–while Gonococci only produce Class I pili. Meningococcal pili are composed of two major pilin families and undergo both phase and antigenic variation:
a. Type IV pili (T4P) are long, hair-like filaments that are helical polymers of one major subunit. It is the major factor for meningococcal adhesion to host cells.
b. Pilin (PilE), produced by the N-terminal cleavage of prepilin by prepilin peptidase PilD. Together with PilV, they promote adhesion to endothelial vessels in vivo. PilE (the product of the pilE gene) is the pilin subunit that assembles into the multifunctional pilus adhesin and virulence factor.
The Surface Exposed Lipoproteins (SLP):
Bacterial lipoproteins are hydrophilic proteins that are anchored to a cell membrane by N-terminally linked fatty acids. They are involved in nutrient acquisition, immune evasion and cellular signaling.
1. NHBA (Neisseria heparin binding antigen, also named GNA2132) is a surface–exposed lipoprotein that is present in all Neisseria meningitidis strains. The antigen induces cross–bactericidal activity in humans and animals and is recognized by sera of patients after meningococcal disease. The protein contains an arginine-rich region that mediates heparin binding in vitro, a property that correlates with increased survival of Neisseria meningitidis in human serum. This evidence suggested the hypothesis that heparin could either mimic other important negatively charged partners or mediate the interaction with factor H and other complement components. It is an outer membrane protein that binds heparin and heparan sulfate and DNA. NHBA is the target of two proteases: the meningococcal NalP and human lactoferrin.
2. fHBP (factor H–binding protein) is a bactericidal surface–exposed lipoprotein able to bind human factor H. The bacterium recruits the negative complement regulator complement factor H (CFH) to its surface by expressing factor H–binding protein (fHbp); this protects the meningococcus from the human complement system.
Other Surface Exposed Lipoproteins:
1. TbpB
– Transferrin binding protein B
2. LbpB
– Lactoferrin binding protein B
3. HpuA
– Haemoglobin-haptoglobin utilization A
4. Ng-MIP
– Macrophage infectivity potentiator
5. AniA
– Anaerobically induced protein A
6. NalP
– Neisseria autotransporter lipoprotein
Disease produced:
The clinical manifestations of meningococcal disease can be classified into (1) bacteremia without sepsis; (2) meningococcemia without meningitis; (3) meningitis with or without meningococcemia and (4) meningoencephalitis. These clinical presentations are not mutually exclusive and often overlap in individual patients and they are more useful as prognostic predictors.
1. Water–Friderichsen syndrome – this syndrome is defined as adrenal failure due to massive hemorrhage into the adrenal glands caused by overwhelming meningococcemia and disseminated intravascular coagulation.
2. Fulminant meningococcal septicemia represents an extreme form of endotoxin–induced sepsis and coagulopathy. The condition is diagnosed clinically by the appearance of hemorrhagic skin lesions and compromised circulation in a febrile patient. The size of the skin lesions can be used, to a certain extent, to predict the clinical severity and the ongoing coagulopathy.
NEISSERIA GONORRHOEAE
Microscopic and clinical morphology resembles Neisseria meningitides but differs in sugar fermentation, antigenic structure, and pathophysiology.
They produce an enzyme carbonic anhydrase that differentiates them from Branhamella species.
Neisseria gonorrhoeae utilizes transferrin as an iron source and its iron acquisition system is composed of two transferrin binding proteins: TbpA and TbpB.
Disease produced:
1. Gonorrhea is a sexually transmitted disease (STD) caused by an infection of Neisseria gonorrhea bacterium. It infects the mucous membranes of the reproductive tract, including the cervix, uterus, and Fallopian Tube of women and the urethra in men and women. It can also infect the mucous membranes of the mouth, throat, eyes, and rectum.
2. Opthalmia neonatorum occurs at birth from passage of the newborn through the mother’s infected cervix and vagina, Crede’s prophylaxis is given – 1% silver nitrate is instilled in the conjunctivitis sac of the newborn.
3. Gonorrheal vulvovaginitis – is usually seen in girls 2 to 8 years of age. The alkaline pH of the prepubertal vagina is cited as one factor favoring the establishment of gonococcal disease and transmitted through contact with fomites.
Virulence factor of Neisseria gonorrhoeae:
1. Type IV Pilus – it mediates the attachment of the bacteria to host cells. Pili aids in overcoming the electrostatic repulsive barrier between the gonococci and host cells as well as adherence to the host cell surface. Pili also plays a role in twitching motility which is accomplished through filament retraction and may provide a mechanism by which non-motile gonococci can colonize and ascend mucosal surfaces. It is also involved in DNA exchange, specifically proteins Pil Q and Pil T. This allows Neisseria gonorrhea to acquire new genes. This is especially dangerous in the clinical setting because it has led to a rise in antibiotic–resistant strains of bacteria.
2. Opacity (Opa) proteins – are a family of integral outer membrane proteins that function as adhesins. Their name refers to the color and opacity changes of bacterial colonies observed with expression of these proteins. Opas are some of the proteins responsible for tight adherence of the bacteria to the host cell surface after the initial attachment of the pili. Two host cell surface molecules have been identified to bind Opas: Heparin Sulfate Proteoglycans (HSPG) and Carcinoembryonic Antigen–related Cell Adhesion Molecules (CEACAMs).
3. Porins – are the most abundant outer membrane protein in the pathogenic Neisseria species. They function as voltage–dependent aqueous pores for the exchange of ions and are essential for bacterial survival. Gonococci only expresses a PorB homolog. The gonoccocal PorB is further classified into two groups, PIA and PIB, based on biochemical and immunological criteria. A unique feature of neisserial porins is their ability to translocate into eukaryotic cell membranes. They act as voltage–gated channels on the target cell surface and are modulated by cytoplasmic ATP and GTP. PorB has been found to cause target cell apoptosis by inducing a rapid calcium influx and activating calpain and caspase activity. In addition, porins act as actin–nucleating proteins in epithelial cells, facilitating cytoskeletal rearrangements and actin-mediated entry of the bacteria. Porins have also been associated with inhibiting phagosome maturation in macrophages as well as neutrophil degranulation, opsonin receptor expression, and phagocytosis. Serum resistance is conferred by porins by down regulating both the classical and alternative complement pathways by binding to the C4b binding protein and factor H, respectively.
4. Lipooligosaccharide (LOS) – the sialylation of LOS contributes to serum resistance by binding factor H and inhibiting alternative complement pathway. However, the presence of sialic acid on LOS also impairs cellular invasion into some cell types, suggesting that LOS variation may allow the gonococci to fluctuate between invasive and serum–resistant phenotypes to promote bacterial survival.
5. Reduction-modifiable protein (Rmp) is a surface exposed outer membrane protein that exhibits a high degree of homology between strains. Rmp was named for the molecular weight shifts observed after SDS-PAGE analysis in reducing conditions and shares partial homology with the enterobacterial OmpA protein. It is intimately associated with porin and LOS in the gonococcal membrane. Antibodies generated against Rmp block binding of antibodies against porin and LOS, inhibiting complement-mediated killing of the gonococci. This impairs the immune response and increases the host susceptibility to infection.
6. IgA1 protease likely only plays a role in immune evasion and intracellular survival of the bacteria.
Enzyme variable Neisseria gonorrhoeae:
1. Penicillinase producing Neisseria gonorrhea (PPNG) – causes the same clinical picture as gonococci but only resistant to penicillin antibiotic. Patients who are PPNG–resistant are treated instead with Spectinomycin.
2. Neisseria gonorrhea Carbonic Anhydrase (NGCA) – the α–carbonic anhydrases were thought to belong exclusively to the eukaryotic world, but it was recently demonstrated that the enzyme from Neisseria gonorrhoeae (NGCA) is of the α type and, thus, homologous to carbonic anhydrases from animal sources.
Laboratory Tests:
1. Oxidase test is carried out by dropping the oxidase reagent (N,N,N,N–tetramethyl–1,4–phenylenediamine dihydrochloride) into the colonies of Neisseria. The colonies will turn black if it is really a Neisseria.
2. Carbohydrate Fermentation test is done to confirm and identify the species. It employs the use of Cysteine Trypticase Soy agar with glucose, maltose & sucrose.
3. Nucleic Acid Amplification Tests (NAATs) are generally more than 95% sensitive and specific in urethral and cervical swabs and first catch urine of males.
4. Detection
of Prolyl Iminopeptidase (PIP) which is an enzyme produced by Neisseria
gonorrhoeae. However, PIP–negative gonococci has emerged thus the combination
of the test with gamma glutamyl transferase (GGT) and butyrate esterase has
been a reliable test panel for identification of pathogenic gonococci.
THE BRANHAMELLA GROUP
Branhamella Group is now known as Moraxella. The pathogenic species in the group is known as Moraxella catarrhalis.
In the original research of Wesley Catlin posit that “the name Branhamella catarrhalis served to distinguish the organism from the so–called nonpathogenic Neisseriae and focused attention on their differing potentials for pathogenicity. The proposed association with Moraxellae, most of which only possess limited pathogenicity would relegate Branhamella catarrhalis to an unfamiliar conglomerate of cocci and rods.” For educational purposes the name Branhamella catarrhalis will still be used in this context.
Characteristics of Branhamella catarrhalis:
1. They are gram negative but tend to resist decolorization.
2. They are catalase–positive, oxidase–positive, aerobic, nonmotile, commonly arranged in pairs with their abutting sides flattened.
3. Their colonies on blood agar are nonhemolytic, circular, grayish white, convex. Colonies when pushed tend to remain intact and slide across the agar like a hockey puck on ice.
4. They are currently recognized as the third most frequent cause of acute otitis media and acute sinusitis in young children. It often causes acute exacerbations of chronic bronchopulmonary disease in older or immunocompromised adults and is incriminated occasionally in meningitis, endocarditis, bacteremia, conjunctivitis, keratitis, and urogenital infections.
5. They are regarded as one of the commonest inhabitants of the pharynx.
6. The beta–lactamase producing strains, first detected in 1976, have risen to approximately 75% worldwide.
7. Branhamella catarrhalis cells possess membrane–associated proteins that bind human lactoferrin and human transferrin thereby enabling the bacteria to utilize these sources of iron for growth.
8. It has also been reported that Branhamella catarrhalis can utilize acetate, lactate, and fatty acids for growth, and several studies have found absolute requirements for different amino acids, including arginine and proline.
9. Branhamella catarrhalis is among a few Gram-negative bacteria with LPS/LOS containing 3-hydroxydodecanoic acid as the sole 3-hydroxy fatty acid.
10. Branhamella can be differentiated from Neisseria biochemically through their positive reaction in tests like:
a. DNase
hydrolysis
b. Nitrate
reduction
c. Tributyrin hydrolysis
4–methylumbelliferyl butyrate and indoxyl butyrate are used in place of tributyrin in other tests for esterase. Release of the 4–methylumbelliferone moiety by hydrolysis is detected by its fluorescence under UV light. Hydrolysis of indoxyl butyrate releases indoxyl, which spontaneously forms indigo blue.
Structure of Branhamella catarrhalis:
1. Pili or Fimbriae – are filamentous appendages that extend from the outer membrane and serve as adhesins.
2. Envelope or Cell wall – consist of two trilaminar structures that have a periplasmic space and a dense peptidoglycan–containing layer.
a. Cytoplasmic membrane (CM) – is the innermost layer, carries penicillin–binding proteins (PBPs) at its outer surface.
b. Outer membrane (OM) – where proteins, lipooligosaccharides (LOS), and phospholipids are found. It should be noted that LOS is a variety of lipopolysaccharide (LPS) that lacks the long, surface–exposed polysaccharide constituting the O antigen of smooth enteric bacteria. The absence of O antigen increases outer membrane permeability, resulting in enhanced susceptibility to erythromycin, rifampin, and other hydrophobic agents. It has eight major outer membrane proteins or OMPs (from OMP–A to OMP–H).
Porins (M35) are proteins that typically exist as trimers forming channels through the outer membrane for passive diffusion of small hydrophilic nutrients and antibiotics.
THE VEILLONELLA GROUP
Characteristics:
1. They are non–fermentative, anaerobic, gram–negative cocci, part of the normal flora of the mouth, gastrointestinal tract, and vaginal tract. They are catalase and oxidase negative. They are also benzidine negative.
2. Their activities are detected within sublingual dental plaque, periodontic infections and osteoarthritic infections.
3. Veillonella species not only coaggregate with various bacteria in the oral cavity but can also optimize the microniche to support the growth of late periodontopathogens, such as Fusobacterium species.
4. They had also been isolated from intravenous drug users with polymicrobial endocarditis.
5. They are rare causes of serious infections such as meningitis, endocarditis, obstructive pneumonitis, prosthetic joint infection, and bacteremia. Bacteremia has been reported almost always in association with an underlying infection such as osteomyelitis.
6. They require lactate for growth but are unable to metabolize normal dietary carbohydrates. Thus, they use lactate produced by other microorganisms and convert it into a range of weaker and probably less cariogenic organic acids, e.g., propionic acid. Methylmalonyl–CoA decarboxylase catalyzes an essential step in the fermentation of lactate.
7. The filter–sterilized sodium salts of fumaric, malic, oxaloacetic, pyruvic, and succinic acids are substitute for lactate as energy sources.
8. The strains grew well in a medium containing Casamino Acids, Lactate, Putrescine, Hypoxanthine, and Vitamins. Growth was not regularly obtained if any of these constituents was deleted from this medium.
9. The presence of Veillonella has been associated with the development of a healthy immune system in infants.
10. Veillonella belongs to the Negativicutes, a diverse clade of bacteria that represent an evolutionary enigma: they phylogenetically belong to Gram-positive (monoderm) Firmicutes yet maintain an outer membrane (OM) with lipopolysaccharide similar to classic Gram-negative (diderm) bacteria. The OMs of Negativicutes have unique characteristics including the replacement of Braun's lipoprotein by OmpM for tethering the OM to the peptidoglycan.
Pathogenic species of Veillonella:
1. Veillonella montpellierensis, has recently been isolated from the gastric fluid of a newborn and from the amniotic fluid of 2 women. Its pathogenic role is still debated.
2. All previously reported cases of Veillonella endocarditis were due to either Veillonella dispar, Veillonella parvula, or Veillonella alcalescens.
3. Veillonella parvula is a biofilm-forming commensal found in the lungs, vagina, mouth, and gastro-intestinal tract of humans, yet it may develop into an opportunistic pathogen.
|
Veillonella
parvula subspecies |
||||||
|
Antigenic group |
Subspecies |
Putrescine |
Cadaverine |
Catalase |
Decompose H2O2 |
Benzidine |
|
I |
criceti |
√ |
√ |
|
√ |
|
|
II |
rodentium |
√ |
√ |
– |
|
|
|
III |
ratti |
x |
x |
|
√ |
|
|
IV |
alcalescence |
√ |
√ |
|
√ |
– |
|
V |
atypica |
x |
x |
– |
|
|
|
VI |
parvula |
x |
x |
|
|
|
|
VII |
dispar |
√ |
√ |
|
√ |
|
Putrescine (butane-1,4–diamine) and cadaverine (pentane–1,5–diamine) are foul–smelling compounds produced when amino acids decompose in decaying animals. They are also found in small amounts in living cells. Putrescine is formed by the decarboxylation of ornithine and arginine; cadaverine by the decarboxylation of lysine.
The production of putrescine, cadaverine and agmatine have extensively been described as used by various bacteria for acid–stress resistance.
Culture Medium & Laboratory Test:
1. Rogosa Medium composed of Trypticase (5g), Yeast Extract (3g), Sodium thioglycollate (750mg), basic fuchsin (0.002g), sodium lactate 50% (25 ml), Tween 80 (1g), Streptomycin (5 ug/ml), pH=7.5
2. In Trypticase–Glucose–Yeast extract (TGY) broth, the metabolic end products are acetic acid and propionic acids. In addition, CO2 and H2 are produced from lactate.
3. Douglas Medium I (for saliva sample)
4. Salts–Yeast–Extract Medium
5. Benzidine test using dihydrochloride is quite satisfactory for detecting the presence of cytochrome–containing respiratory systems in bacteria. The test is a superior criterion in differentiating lactic acid bacteria. Porphyrin test is the alternative test for Benzidine Test.
MEGASPHAERA GROUP
Megasphaera phylotypes 1 and 2 (MP1, MP2) have been associated with bacterial vaginosis (BV) and related adverse reproductive health sequelae. However, these taxa had not previously been characterized beyond their 16S rRNA genes and associations.
Megasphaera species are Gram-negative, with a peculiar diderm cell wall structure typical for the Negativicutes, obligate anaerobes that are often detected in intestinal environments.
Some strain Megasphaera species displayed the
ability to adhere and self-aggregate, which are essential requisite features
for inhabiting and persisting in oral cavity.
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