Neisseria meningitidis

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Neisseria meningitidis
Neisseria meningitidis Charles-Orszag 2018.png
Scanning electron micrograph of a single N. meningitidis cell (colorized in blue) with its adhesive pili (colorized in yellow). The scale bar corresponds to 1 µm.
Scientific classification Red Pencil Icon.png
Domain: Bacteria
Phylum: Proteobacteria
Class: Betaproteobacteria
Order: Neisseriales
Family: Neisseriaceae
Genus: Neisseria
N. meningitidis
Binomial name
Neisseria meningitidis
Albrecht & Ghon 1901

Neisseria meningitidis, often referred to as meningococcus, is a Gram-negative bacterium that can cause meningitis and other forms of meningococcal disease such as meningococcemia, a life-threatening sepsis. It has also been reported to be transmitted through oral sex and cause urethritis in men. [1] The bacterium is referred to as a coccus because it is round, and more specifically, diplococcus because of its tendency to form pairs. About 10% of adults are carriers of the bacteria in their nasopharynx. [2] As an exclusively human pathogen it is the main cause of bacterial meningitis in children and young adults, causing developmental impairment and death in about 10% of cases. It causes the only form of bacterial meningitis known to occur epidemically, mainly Africa and Asia. It occurs worldwide in both epidemic and endemic form. [3] N. meningitidis is spread through saliva and respiratory secretions during coughing, sneezing, kissing, chewing on toys and even through sharing a source of fresh water. It infects its host cells by sticking to them with long thin extensions called pili and the surface-exposed proteins Opa and Opc and has several virulence factors.

Gram-negative bacteria group of bacteria that do not retain the crystal violet stain used in the Gram staining method of bacterial differentiation

Gram-negative bacteria are bacteria that do not retain the crystal violet stain used in the gram-staining method of bacterial differentiation. They are characterized by their cell envelopes, which are composed of a thin peptidoglycan cell wall sandwiched between an inner cytoplasmic cell membrane and a bacterial outer membrane.

Meningitis inflammation of membranes around the brain and spinal cord

Meningitis is an acute inflammation of the protective membranes covering the brain and spinal cord, known collectively as the meninges. The most common symptoms are fever, headache, and neck stiffness. Other symptoms include confusion or altered consciousness, vomiting, and an inability to tolerate light or loud noises. Young children often exhibit only nonspecific symptoms, such as irritability, drowsiness, or poor feeding. If a rash is present, it may indicate a particular cause of meningitis; for instance, meningitis caused by meningococcal bacteria may be accompanied by a characteristic rash.

Meningococcal disease Human disease

Meningococcal disease describes infections caused by the bacterium Neisseria meningitidis. It has a high mortality rate if untreated but is vaccine-preventable. While best known as a cause of meningitis, it can also result in sepsis, which is an even more damaging and dangerous condition. Meningitis and meningococcemia are major causes of illness, death, and disability in both developed and under-developed countries.


Signs and symptoms

Meningococcus can cause meningitis and other forms of meningococcal disease. [4] It initially produces general symptoms like fatigue, fever, and headache and can rapidly progress to neck stiffness, coma and death in 10% of cases. Symptoms of meningococcal meningitis are easily confused with those caused by other bacteria, such as Haemophilus influenzae and Streptococcus pneumoniae . [5] [6] Suspicion of meningitis is a medical emergency and immediate medical assessment is recommended. Current guidance in the United Kingdom is that if a case of meningococcal meningitis or septicaemia (infection of the blood) is suspected intravenous antibiotics should be given and the ill person admitted to the hospital. [7] This means that laboratory tests may be less likely to confirm the presence of Neisseria meningitidis as the antibiotics will dramatically lower the number of bacteria in the body. The UK guidance is based on the idea that the reduced ability to identify the bacteria is outweighed by reduced chance of death.

Neck stiffness, stiff neck and nuchal rigidity are terms often used interchangeably to describe the medical condition when one experiences discomfort or pain when trying to turn, move, or flex the neck. Possible causes include muscle strain or sprain, cervical spine disorders, meningitis, and subarachnoid hemorrhage.

<i>Haemophilus influenzae</i> species of bacterium

Haemophilus influenzae is a Gram-negative, coccobacillary, facultatively anaerobic pathogenic bacterium belonging to the Pasteurellaceae family. H. influenzae was first described in 1892 by Richard Pfeiffer during an influenza pandemic.

<i>Streptococcus pneumoniae</i> species of bacterium

Streptococcus pneumoniae, or pneumococcus, is a Gram-positive, alpha-hemolytic or beta-hemolytic, facultative anaerobic member of the genus Streptococcus. They are usually found in pairs (diplococci) and do not form spores and are nonmotile. As a significant human pathogenic bacterium S. pneumoniae was recognized as a major cause of pneumonia in the late 19th century, and is the subject of many humoral immunity studies.

Septicaemia caused by Neisseria meningitidis has received much less public attention than meningococcal meningitis even though septicaemia has been linked to infant deaths. [8] Meningococcal septicaemia typically causes a purpuric rash, that does not lose its color when pressed with a glass ("non-blanching") and does not cause the classical symptoms of meningitis. This means the condition may be ignored by those not aware of the significance of the rash. Septicaemia carries an approximate 50% mortality rate over a few hours from initial onset.

Non-blanching rash

A non-blanching rash (NBR) is a skin rash that does not fade when pressed with, and viewed through, a glass.

Mortality rate measure of the number of deaths in a population

Mortality rate, or death rate, is a measure of the number of deaths in a particular population, scaled to the size of that population, per unit of time. Mortality rate is typically expressed in units of deaths per 1,000 individuals per year; thus, a mortality rate of 9.5 in a population of 1,000 would mean 9.5 deaths per year in that entire population, or 0.95% out of the total. It is distinct from "morbidity", which is either the prevalence or incidence of a disease, and also from the incidence rate.

Other severe complications include Waterhouse–Friderichsen syndrome, a massive, usually bilateral, hemorrhage into the adrenal glands caused by fulminant meningococcemia, adrenal insufficiency, and disseminated intravascular coagulation. [6]

Waterhouse–Friderichsen syndrome (WFS) is defined as adrenal gland failure due to bleeding into the adrenal glands, commonly caused by severe bacterial infection: Typically it is caused by Neisseria meningitidis.

Adrenal insufficiency human disease

Adrenal insufficiency is a condition in which the adrenal glands do not produce adequate amounts of steroid hormones, primarily cortisol; but may also include impaired production of aldosterone, which regulates sodium conservation, potassium secretion, and water retention. Craving for salt or salty foods due to the urinary losses of sodium is common.

Disseminated intravascular coagulation pathological process characterized by the widespread activation of the clotting cascade that results in the formation of blood clots in the small blood vessels throughout the body

Disseminated intravascular coagulation (DIC) is a condition in which blood clots form throughout the body, blocking small blood vessels. Symptoms may include chest pain, shortness of breath, leg pain, problems speaking, or problems moving parts of the body. As clotting factors and platelets are used up, bleeding may occur. This may include blood in the urine, blood in the stool, or bleeding into the skin. Complications may include organ failure.

Not all instances of a purpura-like rash are due to meningococcal septicaemia; other possible causes, such as idiopathic thrombocytopenic purpura (ITP; a platelet disorder) and Henoch–Schönlein purpura, also need prompt investigation.

Purpura human disease

Purpura is a condition of red or purple discolored spots on the skin that do not blanch on applying pressure. The spots are caused by bleeding underneath the skin secondary to platelet disorders, vascular disorders, coagulation disorders, or other causes. They measure 0.3–1 cm (3–10 mm), whereas petechiae measure less than 3 mm, and ecchymoses greater than 1 cm.

Platelet component of blood

Platelets, also called thrombocytes, are a component of blood whose function is to react to bleeding from blood vessel injury by clumping, thereby initiating a blood clot. Platelets have no cell nucleus: they are fragments of cytoplasm that are derived from the megakaryocytes of the bone marrow, and then enter the circulation. Circulating unactivated platelets are biconvex discoid (lens-shaped) structures, 2–3 µm in greatest diameter. Activated platelets have cell membrane projections covering their surface. Platelets are found only in mammals, whereas in other animals thrombocytes circulate as intact mononuclear cells.

Henoch–Schönlein purpura Human disease

Henoch–Schönlein purpura (HSP) is a disease of the skin, mucous membranes, and sometimes other organs that most commonly affects children. In the skin, the disease causes palpable purpura, often with joint pain and abdominal pain. With kidney involvement, there may be a loss of small amounts of blood and protein in the urine, but this usually goes unnoticed; in a small proportion of cases, the kidney involvement proceeds to chronic kidney disease. HSP is often preceded by an infection, such as a throat infection.


N. meningitidis is a Gram-negative diplococcus since it has an outer and inner membranes with a thin layer of peptidoglycan in between. It is 0.6–1.0 micrometers in size. It tests positive for the enzyme cytochrome c oxidase. [9]

Peptidoglycan, also known as murein, is a polymer consisting of sugars and amino acids that forms a mesh-like layer outside the plasma membrane of most bacteria, forming the cell wall. The sugar component consists of alternating residues of β-(1,4) linked N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM). Attached to the N-acetylmuramic acid is a peptide chain of three to five amino acids. The peptide chain can be cross-linked to the peptide chain of another strand forming the 3D mesh-like layer. Peptidoglycan serves a structural role in the bacterial cell wall, giving structural strength, as well as counteracting the osmotic pressure of the cytoplasm. Peptidoglycan is also involved in binary fission during bacterial cell reproduction.

Cytochrome c oxidase enzyme

The enzyme cytochrome c oxidase or Complex IV, EC is a large transmembrane protein complex found in bacteria, archaea, and in eukaryotes in their mitochondria.


N. meningitidis is a part of the normal nonpathogenic flora in the nasopharynx of up to 5–15% of adults. [10] It colonizes and infects only humans, and has never been isolated from other animals. This is thought to stem from the bacterium's inability to get iron from sources other than human transferrin and lactoferrin. [5]


Disease-causing strains are classified according to the antigenic structure of their polysaccharide capsule. [11] Serotype distribution varies markedly around the world. [12] Among the 13 identified capsular types of N. meningitidis, six (A, B, C, W135, X, and Y) account for most disease cases worldwide. [13] Type A has been the most prevalent in Africa and Asia, but is rare/practically absent in North America. In the United States, serogroup B is the predominant cause of disease and mortality, followed by serogroup C. The multiple subtypes have hindered development of a universal vaccine for meningococcal disease.



Lipooligosaccharide (LOS) is a component of the outer membrane of N. meningitidis. This acts as an endotoxin and is responsible for septic shock and hemorrhage due to the destruction of red blood cells. [14] Other virulence factors include a polysaccharide capsule which prevents host phagocytosis and aids in evasion of the host immune response; fimbriae mediate attachment of the bacterium to the epithelial cells of the nasopharynx. [15] [16] It infects the cell by sticking to it mainly with long thin extensions called pili and the surface-exposed proteins Opa and Opc. [17] Meningococci produce an IgA protease, an enzyme that cleaves IgA class antibodies and thus allows the bacteria to evade a subclass of the humoral immune system.

A hypervirulent strain was discovered in China. Its impact is yet to be determined. [6]

Complement inhibition

Factor H binding protein (fHbp) that is exhibited in N. meningitidis and some commensal species is the main inhibitor of the alternative complement pathway. fHbp protects meningococci from complement-mediated death in human serum experiments, but has also been shown to protect meningococci from antimicrobial peptides in vitro. Factor H binding protein is key to the pathogenesis of N. meningitidis, and is, therefore, important as a potential vaccine candidate. [18] Porins are also an important factor for complement inhibition for both pathogenic and commensal species. Porins are important for nutrient acquisition. Porins are also recognized by TLR2, they bind complement factors (C3b, C4b, factor H, and C4bp (complement factor 4b-binding protein)). Cooperation with pili for CR3-mediated internalization is another function of porins. Ability to translocate into host cells and modulate reactive oxygen species production and apoptosis is made possible by porins, as well. Strains of the same species can express different porins.


At least 8 complete genomes of Neisseria meningitidis strains have been determined which encode about 2,100 to 2,500 proteins. [19]

The genome of strain MC58 (serogroup B) has 2,272,351-base pairs. When sequenced in 2000, it was found to contain 2158 open reading frames (ORFs). Of these, a biological function was predicted for 1158 (53.7%). There were three major islands of horizontal DNA transfer found. Two encode proteins involved in pathogenicity. The third island only codes for hypothetical proteins. They also found more genes that undergo phase variation than any pathogen then known. Phase variation is a mechanism that helps the pathogen to evade the immune system of the host. [20]

The genome size of strain H44/76 is 2.18 Mb, and encodes 2,480 open reading frames (ORFs), compared to 2.27 Mb and 2,465 ORFs for MC58. [19] Both strains have a GC content of 51.5%. [19] A comparison with MC58 showed that four genes are uniquely present in H44/76 and nine genes are only present in MC58. Of all ORFs in H44/76, 2,317 (93%) show more than 99% sequence identity. [19]

The complete genome sequence of strain NMA510612 (serogroup A) consists of one circular chromosome with a size of 2,188,020 bp, and the average GC content is 51.5%. The chromosome is predicted to possess 4 rRNA operons, 163 insertion elements (IS), 59 tRNAs, and 2,462 ORFs. [21]

Genetic transformation

Genetic transformation is the process by which a recipient bacterial cell takes up DNA from a neighboring cell and integrates this DNA into the recipient’s genome by recombination. In N. meningitidis, DNA transformation requires the presence of short DNA sequences (9–10 mers residing in coding regions) of the donor DNA. These sequences are called DNA uptake sequences (DUSs). Specific recognition of these sequences is mediated by a type IV pilin. [22] In N. meningitidis DUSs occur at a significantly higher density in genes involved in DNA repair and recombination (as well as in restriction-modification and replication) than in other annotated gene groups. The over-representation of DUS in DNA repair and recombination genes may reflect the benefit of maintaining the integrity of the DNA repair and recombination machinery by preferentially taking up genome maintenance genes, that could replace their damaged counterparts in the recipient cell. [23]

N. meningititis colonizes the nasopharyngeal mucosa, which is rich in macrophages. Upon their activation, macrophages produce superoxide (O2¯) and hydrogen peroxide (H2O2). Thus N. meningitidis is likely to encounter oxidative stress during its life cycle. [24] Consequently, an important benefit of genetic transformation to N. meningitidis may be the maintenance of the recombination and repair machinery of the cell that removes oxidative DNA damages such as those caused by reactive oxygen. This is consistent with the more general idea that transformation benefits bacterial pathogens by facilitating repair of DNA damages produced by the oxidative defenses of the host during infection. [25]


The growth of Neisseria meningitidis colonies on New York City agar Neisseria meningitidis Colonies growth on New York City Medium Agar.jpg
The growth of Neisseria meningitidis colonies on New York City agar
Neisseria meningitidis in cerebrospinal fluid (CSF) seen by Gram stain at 1000x magnification Neisseria meningitidis CSF Gram 1000.jpg
Neisseria meningitidis in cerebrospinal fluid (CSF) seen by Gram stain at 1000x magnification

With a fatality risk approaching 15% within 12 hours of infection, it is crucial to initiate testing as quickly as possible, but not to wait for the results before initiating antibiotic therapy.

A small amount of cerebrospinal fluid (CSF) is sent to the laboratory as soon as possible for analysis. The diagnosis is suspected, when Gram-negative diplococci are seen on Gram stain of a centrifuged sample of CSF; sometimes they are located inside white blood cells. The microscopic identification takes around 1–2 hours after specimen arrival in the laboratory. [4]

The gold standard of diagnosis is microbiological isolation of N. meningitidis by growth from a sterile body fluid, which could be CSF or blood. [6] Diagnosis is confirmed when the organism has grown, most often on a chocolate agar plate, but also on Thayer-Martin agar. To differentiate any bacterial growth from other species a small amount of a bacterial colony is tested for oxidase, catalase for which all clinically relevant Neisseria show a positive reaction, and the carbohydrates maltose, sucrose, and glucose, in which N. meningitidis will ferment that is, utilize the glucose and maltose. Finally, serology determines the subgroup of the N. meningitidis, which is important for epidemiological surveillance purposes; this may often only be done in specialized laboratories.

The above tests take a minimum of 48–72 hours turnaround time for growing the organism, and up to a week more for serotyping. Growth can and often does fail, either because antibiotics have been given preemptively, or because specimens have been inappropriately transported, as the organism is extremely susceptible to antibiotics and fastidious in its temperature, CO
and growth medium requirements.

Polymerase chain reaction (PCR) tests where available, mostly in industrialized countries, have been increasingly used; PCR can rapidly identify the organism, and works even after antibiotics have been given. [6]


All recent contacts of the infected patient over the 7 days before onset should receive medication to prevent them from contracting the infection. This especially includes young children and their child caregivers or nursery-school contacts, as well as anyone who had direct exposure to the patient through kissing, sharing utensils, or medical interventions such as mouth-to-mouth resuscitation. Anyone who frequently ate, slept or stayed at the patient's home during the 7 days before the onset of symptom, or those who sat beside the patient on an airplane flight or classroom for 8 hours or longer, should also receive chemoprophylaxis. The agent of choice is usually oral rifampicin for a few days. [6]

Receiving a dose of the Meningococcal vaccine before traveling to a country in the "meningitis belt" or having a booster meningitis vaccine, normally five years apart could prevent someone from getting an infection from the pathogen. [26]


United States

A number of vaccines are available in the U.S. to prevent meningococcal disease. Some of the vaccines cover serogroup B, while others cover A, C, W, and Y. [27] A meningococcal polysaccharide vaccine (MPSV4) has been available since the 1970s and is the only meningococcal vaccine licensed for people older than 55. MPSV4 may be used in people 2–55 years old if the MCV4 vaccines are not available or contraindicated. Two meningococcal conjugate vaccines (MCV4) are licensed for use in the U.S. The first conjugate vaccine was licensed in 2005, the second in 2010. Conjugate vaccines are the preferred vaccine for people 2 through 55 years of age. It is indicated in those with impaired immunity, such as nephrotic syndrome or splenectomy. The Centers for Disease Control and Prevention (CDC) publishes information about who should receive meningococcal vaccine. [28]

In June 2012, the U.S. Food and Drug Administration (FDA) approved a combination vaccine against two types of meningococcal diseases and Hib disease for infants and children 6 weeks to 18 months old. The vaccine, Menhibrix, was designed to prevent disease caused by Neisseria meningitidis serogroups C and Y, and Haemophilus influenzae type b (Hib). It was the first meningococcal vaccine that could be given to infants as young as six weeks old. [29]

In October 2014 the FDA approved the first vaccine effective against serogroup B, named Trumenba, for use in 10- to 25-year-old individuals. [30]


In 2010, the Meningitis Vaccine Project introduced a vaccine called MenAfriVac in the African meningitis belt. It was made by generic drug maker Serum Institute of India and cost 50 U.S. cents per injection. Beginning in Burkina Faso in 2010, it has been given to 215 million people across Benin, Cameroon, Chad, Ivory Coast, Ethiopia, Ghana, Mali, Niger, Mauritania, Nigeria, Senegal, Sudan, Togo and Gambia. [31] The vaccination campaign has resulted in near-elimination of serogroup A meningitis from the participating countries. [32]


Persons with confirmed N. meningitidis infection should be hospitalized immediately for treatment with antibiotics. Because meningococcal disease can disseminate very rapidly, a single dose of intramuscular antibiotic is often given at the earliest possible opportunity, even before hospitalization, if disease symptoms look suspicious enough. [6] Third-generation cephalosporin antibiotics (i.e. cefotaxime, ceftriaxone) should be used to treat a suspected or culture-proven meningococcal infection before antibiotic susceptibility results are available. [33] Empirical treatment should also be considered if a lumbar puncture, to collect CSF for laboratory testing, cannot be done within 30 minutes of admission to hospital. [34] [35] Antibiotic treatment may affect the results of microbiology tests, but a diagnosis may be made on the basis of blood-cultures and clinical examination. [36]


N. meningitidis is a major cause of illness, developmental impairment and death during childhood in industrialized countries and has been responsible for epidemics in Africa and in Asia. Every year, about 2,500 to 3,500 people become infected with N. meningitidis in the US, with a frequency of about 1 in 100,000. Children younger than 5 years are at greatest risk, followed by teenagers of high school age. Rates in the African meningitis belt were as high as 1 in 1,000 to 1 in 100 [6] before introduction of a vaccine in 2010. The incidence of meningococcal disease is highest among infants (children younger than 1-year-old) whose immune system is relatively immature. In industrialized countries there is a second peak of incidence in young adults, who are congregating closely, living in dormitories or smoking. [37] Vaccine development is ongoing. [38] It is spread through saliva and other respiratory secretions during coughing, sneezing, kissing, and chewing on toys. Inhalation of respiratory droplets from a carrier which may be someone who is themselves in the early stages of disease can transmit the bacteria. Close contact with a carrier is the predominant risk factor. Other risk factors include a weakened general or local immune response, such as a recent upper respiratory infection, smoking, and complement deficiency. The incubation period is short, from 2 to 10 days. In susceptible individuals, N. meningitidis may invade the bloodstream and cause a systemic infection, sepsis, disseminated intravascular coagulation, breakdown of circulation, and septic shock.


In 1884 Ettore Marchiafava and Angelo Celli first observed the bacterium inside cells in the cerebral spinal fluid (CSF). [39] In 1887 Anton Weichselbaum isolated the bacterium from the CSF of patients with bacterial meningitis. [40] He named the bacterium Diplococcus intracellularis meningitidis. [39]

See also

Related Research Articles


A pilus is a hair-like appendage found on the surface of many bacteria. The terms pilus and fimbria can be used interchangeably, although some researchers reserve the term pilus for the appendage required for bacterial conjugation. All pili in the latter sense are primarily composed of pilin proteins, which are oligomeric.

<i>Escherichia coli</i> species of Gram-negative, rod-shaped bacterium

Escherichia coli, also known as E. coli, is a Gram-negative, facultative anaerobic, rod-shaped, coliform bacterium of the genus Escherichia that is commonly found in the lower intestine of warm-blooded organisms (endotherms). Most E. coli strains are harmless, but some serotypes can cause serious food poisoning in their hosts, and are occasionally responsible for product recalls due to food contamination. The harmless strains are part of the normal microbiota of the gut, and can benefit their hosts by producing vitamin K2, and preventing colonization of the intestine with pathogenic bacteria, having a symbiotic relationship. E. coli is expelled into the environment within fecal matter. The bacterium grows massively in fresh fecal matter under aerobic conditions for 3 days, but its numbers decline slowly afterwards.

<i>Vibrio cholerae</i> species of bacterium

Vibrio cholerae is a Gram-negative, comma-shaped bacterium. The bacterium's natural habitat is brackish or saltwater. Some strains of V. cholerae cause the disease cholera. V. cholerae is a facultative anaerobe and has a flagellum at one cell pole as well as pili. V. cholerae can undergo respiratory and fermentative metabolism. When ingested, V. cholerae can cause diarrhoea and vomiting in a host within several hours to 2–3 days of ingestion. V. cholerae was first isolated as the cause of cholera by Italian anatomist Filippo Pacini in 1854, but his discovery was not widely known until Robert Koch, working independently 30 years later, publicized the knowledge and the means of fighting the disease.

<i>Neisseria gonorrhoeae</i> species of bacterium

Neisseria gonorrhoeae, also known as gonococcus (singular), or gonococci (plural) is a species of Gram-negative diplococci bacteria isolated by Albert Neisser in 1879. It causes the sexually transmitted genitourinary infection gonorrhea as well as other forms of gonococcal disease including disseminated gonococcemia, septic arthritis, and gonococcal ophthalmia neonatorum.

<i>Neisseria</i> genus of bacteria

Neisseria is a large genus of bacteria that colonize the mucosal surfaces of many animals. Of the 11 species that colonize humans, only two are pathogens, N. meningitidis and N. gonorrhoeae. Most gonoccocal infections are asymptomatic and self-resolving, and epidemic strains of the meningococcus may be carried in >95% of a population where systemic disease occurs at <1% prevalence.

MeNZB was a vaccine against a specific strain of group B meningococcus, used to control an epidemic of meningococcal disease in New Zealand. Most people are able to carry the meningococcus bacteria safely with no ill effects. However, meningococcal disease can cause meningitis and septicaemia, resulting in brain damage, failure of various organs, severe skin and soft-tissue damage, and death.

Bacterial capsule

The bacterial capsule is a very large structure of many bacteria. It is a polysaccharide layer that lies outside the cell envelope, and is thus deemed part of the outer envelope of a bacterial cell. It is a well-organized layer, not easily washed off, and it can be the cause of various diseases.

Rino Rappuoli American medical researcher

Rino Rappuoli is Chief Scientist & Head of External Research and Development (R&D) at GlaxoSmithKline (GSK) Vaccines. Previously, he has served as visiting scientist at Rockefeller University and Harvard Medical School and held roles at Sclavo, Vaccine Research and CSO, Chiron Corporation, and Novartis Vaccines.

Pasteurella multocida is a Gram-negative, nonmotile, penicillin-sensitive coccobacillus belonging to the Pasteurellaceae family. Strains belonging to the species are currently classified into five serogroups based on capsular composition and 16 somatic serovars (1-16). P. multocida is the cause of a range of diseases in mammals and birds, including fowl cholera in poultry, atrophic rhinitis in pigs, and bovine hemorrhagic septicemia in cattle and buffalo. It can also cause a zoonotic infection in humans, which typically is a result of bites or scratches from domestic pets. Many mammals and birds harbor it as part of their normal respiratory microbiota.

George D. Heist (1886–1920) was an immunologist specializing in the study of infections of meningococcal bacteria that often result in meningococcal disease, which is well known as highly lethal and debilitating, and extremely difficult to treat.

Neisseria lactamica is a gram-negative diplococcus bacterium. It is strictly a commensal species of the nasopharynx. Uniquely among the Neisseria they are able to produce β-D-galactosidase and ferment lactose.


NmVac4-A/C/Y/W-135 is the commercial name of the Meningococcal meningitis polysaccharide serogroups A,C,Y and W-135 vaccine of JN-International Medical Corporation. The product is specially designed and formulated to be used in developing countries for protecting populations during meningitis disease epidemics. Meningococcal meningitis is a bacterial infection caused by the bacterium Neisseria meningitidis, also known as meningococcus. The vaccine is made from bacterial capsular polysaccharides through fermentation of each individual serogroup of Neisseria meningitidis in bioreactors. Then the polysaccharides are purified, formulated and lyophilized using preservatives and stabilizers to make a vaccine product. The vaccine cannot protect other than Neisseria meningitidis serogroups A,C,Y and W-135 or cannot completely protect from these serogroups.

Meningococcal vaccine refers to any of the vaccines used to prevent infection by Neisseria meningitidis. Different versions are effective against some or all of the following types of meningococcus: A, B, C, W-135, and Y. The vaccines are between 85 and 100% effective for at least two years. They result in a decrease in meningitis and sepsis among populations where they are widely used. They are given either by injection into a muscle or just under the skin.

MenAfriVac is a vaccine developed for use in sub-Saharan Africa for children and adults between 9 months and 29 years of age against meningococcal bacterium Neisseria meningitidis group A. The vaccine costs less than US$0.50 per dose.

Antibiotic resistance in gonorrhea

The Gonorrhea bacterium Neisseria gonorrhoeae has developed antibiotic resistance to many antibiotics.

Natasha Anwar is a Molecular Biologist born in Britain to Pakistani parents. She completed her education in London at the Imperial College of Science Technology and Medicine, getting a PhD in Molecular Biology. Soon after she moved back to her home in Lahore, Pakistan, she began conducting her research at Shaukat Khanum Memorial Cancer Hospital and Research Centre focusing mainly on health issues specific to the Pakistani population. She became a professor at the Froman Christian College in 2011 and has also partnered with biotechnology companies and is now partaking in research on tuberculosis and viral infections.


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