Gram-negative diplococci. N. cinerea, N. gonorrhea, N. lactamica, N. meningitis (Serogroups A, B, C, W135 in US. X in Africa. E in Austrailia.), N. subflava, N. sicca.

On gram stain Neisseria are side to side footballs, streptococci tend to be end to end footballs.

Some gonorrhea lacks the prolyliminopeptidase and as a result, may not have a positive antigen test (PubMed).

Culture and nucleic acid amplification (NAAT) are the way to make the diagnosis.

Epidemiologic Risks

N. gonorrhoeae: sex with an infected partner. If you blame acquisition on a toilet seat, all I can say is that's a hell of a place to have sex. Neonates can acquire it at birth.

Getting ready for a date? Listerine (which does NOT contain Listeria) can kill oral GC (PubMed). Men who have sex with men have markedly more transmission; perhaps they should use Listerine? (PubMed).

Newly single men (not women) asking for ED (erectile dysfunction, not emergency department) meds are at risk and the rates go up with eviction (PubMed).

There was a cluster of oropharyngeal gonorrhea in the absence of urogenital gonorrhea transmitted by tongue kissing (Pubmed).

N. meningitidis: can be part of normal flora, especially in the winter and during times of crowding. Carriage rates depends on age: "Carriage prevalence increased through childhood from 4·5% in infants to a peak of 23·7% in 19-year olds and subsequently decreased in adulthood to 7·8% in 50-year olds. The odds of testing positive for carriage decreased if swabs were not plated immediately after being taken compared with if swabs were plated immediately (PubMed)"

A "mutation in SPLUNC1 affecting mucosal attachment, biofilm formation, and invasion of mucosal epithelial cells is a new genetic cause of meningococcal disease (Pubmed).

MSM have increased rates of N. meningitidis and HIV positive MSM even more (PubMed).

Females may be more likely to die (PubMed).

Terminal complement deficiency (PubMed) is a risk as is the use of Eculizumab a terminal complement inhibitor used to treat paroxysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndrome (aHUS), including an increased risk for DGI (PubMed).

N. lactamica, N. sicca, N. subflava, N. cinerea: part of normal human flora.

7% of patients under age 40 with bacteremia from Streptococcus pneumoniae, Streptococcus pyogenes group A, Neisseria meningitidis, Neisseria gonorrhoeae, or Haemophilus influenzae will die and 25% will be readmitted in the subsequent two years. They have immunologic issues: low immunoglobulins or a complement deficiency (Pubmed).


N. gonorrhoeae: urethritis, cervicitis, disseminated disease with a migratory tenosynovitis followed by oligoarticular arthritis (with and without a purpuric rash), PID, occasionally pharyngitis (not uncommon in men who have sex with men but 95% are asymptomatic (PubMed)), and proctitis.

Patients can present with acute abdominal pain that leads to surgery (PubMed). I have seen such a presentation myself. This presentation tends to be hyper-virulent strains, type W, and with a high mortality rate.

When testing one orifice, remember to test them all (PubMed).

In men who have sex with men, GC can be often found in the pharynx and routine therapy for urethral diseases may not eradicate it (PubMed).

N. meningitidis: meningitis and sepsis with and without purpura. About 8% will develop arthritis (clinically making you wonder if GC) that will respond to antibiotics and a tap without taking to the OR, although the fact that many needed steroids to get better suggests better debridement may have been in order (PubMed). HIV patients have 10 x the incidence of disease (Pubmed).

W is different: "Compared with other serogroups, IMD-W patients were diagnosed more often with septicemia (46%) or pneumonia (12%) and less often with meningitis (17%, P < .001). IMD-W cases presented more often with respiratory symptoms (45%, P < .001); 16% of IMD-W patients presented with diarrhea without IMD-specific symptoms (P = .061) (Pubmed).

This is a rare, chronic, form of the disease (PubMed).

And Neisseria meningitidis sequence type 11 is a cause urethritis in MSM with oral-genital transmission (PubMed)(PubMed) and proctitis (PubMed).

N. lactamica, N. sicca, N. subflava, N. cinerea: will be isolated in sputum, blood and other body fluids on occasion, significance depends on the patient and the body fluid. I see the occasional endocarditis with these Neisseria.


N. gonorrhoeae

N. gonorrhoeae is well on its way to becoming the first completely resistant common pathogen (Pubmed). I bet it beats S. aureus to the punch. Here is a nice review of Neisseria antibiotic evolution (PubMed).

N. gonorrhoeae: All from the CDC STD Guidelines of 2015 except as noted (CDC).

Resistance is climbing in Asia Pacific (Pubmed).

MSM seems a particular risk for resistance.

Given resistance rates, YOU CANNOT USE quinolones for GC and rely on it (PubMed). GC can become resistant to azithromycin in as little as 12 days after exposure. And azithromycin resistance is increasing as well (PubMed), like in England (PubMed). Antibiotic resistance by STD always seems to be reported in areas where people like to go for a vacation like Hawaii. Must be intense evolutionary pressure.

As of Oct 2015, the CDC recommends dual therapy with a cephalosporin (ceftriaxone; 500 mg IM) plus either azithromycin (preferred) or doxycycline because of increasing resistance including resistance of cefixime; there is now a strain resistant to all antibiotics except the carbapenems (PubMed).

No more po treatments: "A 400-mg oral dose of cefixime should only be considered as an alternative cephalosporin regimen because it does not provide as high, nor as sustained, bactericidal blood levels as a 500-mg dose of ceftriaxone; further, it demonstrates limited efficacy for treatment of pharyngeal gonorrhea"

Uncomplicated Gonococcal Infections of the Cervix, Urethra, and Rectum

Recommended Regimens (CDC)*

ceftriaxone 500 mg IM in a single dose. Preferred. Resistance reported in Asia and Canada (PubMed).

As of Aug 2012, no more po cephalosporins to treat GC. Too much resistance.


azithromycin 1g orally in a single dose


doxycycline 100 mg a day for 7 days

As back up, but not CDC approved, consider gentamicin 240 mg intramuscularly plus azithromycin  2 g orally (100% cure), although the gentamicin may not eradicate gc in the pharynx PubMed OR gemifloxacin 320 mg orally plus azithromycin 2 g orally (98.5% cure) (PubMed).

Uncomplicated Gonococcal Infections of the Pharynx

ceftriaxone 500 mg IM in a single dose. Preferred.


azithromycin 1g orally in a single dose.


doxycycline 100 mg a day for 7 days. However, the doxycycline option may have a higher failure rate (PubMed).

* Quinolones should not be used for infections in MSM or in those with a history of recent foreign travel or partners’ travel, infections acquired in California or Hawaii, or infections acquired in other areas with increased QRNG prevalence.

Recommended Regimens for MSM or Heterosexuals with a History of Recent Travel*

Ceftriaxone 500 mg IM in a single dose.



* Quinolones should not be used for infections in MSM or in those with a history of recent foreign travel or partners’ travel, infections acquired in California or Hawaii, or infections acquired in other areas with increased QRNG prevalence.

As of 2003, 14% are resistant to penicillin and 6.5% are resistant to tetracycline (PubMed).

As of 2010, there is decreased susceptibility to azithromycin reported in SoCal (PubMed).

Disseminated Gonococcal Infection (DGI) Recommended Regimen:

Ceftriaxone 1 g IM or IV every 24 hours


Cefotaxime 1 g IV every 8 hours


Ceftizoxime 1 g IV every 8 hours

All of the preceding regimens with a single gram of azithromycin and should be continued for 24--48 hours after improvement begins, at which time therapy can be switched to cefixime 400 mg orally twice daily to complete at least 1 week of antimicrobial therapy. No treatment failures have been reported with the recommended regimens.

Whenever you treat GC, you treat chlamydia and vice versa.

- one alternative for GC is gentamicin 240 mg intramuscularly plus azithromycin 2 g orally, or gemifloxacin 320 mg orally plus azithromycin 2 g orally (PubMed).

For resistant GC, there is Zoliflodacin (PubMed) in the pipeline. And, no, it is not "metal as f–k" as Ars Technica would have you believe. I have added "metal as f–k" to the list of 'strong', 'big gun' and 'powerful': adjectives that mark the speaker as someone who is the Jon Snow of Infectious Diseases.

And gentamicin? Single 240 mg dose inferior (PubMed). So it is not a good alternative if issues with resistance or allergies.

90% will be symptom free a week after therapy, if they have Chlamydia it may take a bit longer (PubMed).

N. meningitidis

N. meningitidis: Penicillin (although resistance is starting to creep up in some parts of the world) OR a third-generation cephalosporin or, if no meningitis, quinolones. While we usually treat for 10 days, 5 may be sufficient.

"Dexamethasone use is safe and can prevent some arthritis episodes, and prophylactic phenytoin might be useful in a selected population. A rapid response and antibiotic therapy may help improve prognosis (PubMed)."

Do not forget steroids if meningitis

Prophylaxis: if they were sharing air with the index case for greater than 4 hours or exchanging body fluids (saliva) or a roommate in a crowded situation (prison or dorms) up to 10 days from onset of index case disease. Rifampin 600 mg po q 12 x 2 d OR ciprofloxacin 500 mg po x 1 OR ceftriaxone 250 mg im x 1 (pregnancy).

BEWARE: there has been quinolone resistance in the US as of 2008 (MMWR) and it may not be the right drug in your area.

Type Y can have penicillin and ciprofloxacin resistance (Pubmed).

Here is my 'take':

Meningococcal Post-Exposure Prophylaxis

There is apparently some misunderstanding about the necessity of post-exposure prophylaxis for health care providers exposed to real or potential cases of Meningococcal meningitis or bacteremia. Exposure to colonized patients is not a risk and can be present in 2%–10% of children and

“In Europe, as much as 35% of young adults are carriers at a given time.”

Family members exposed to an index case of invasive disease are transiently at increased risk for disease with an attack rate of .3 to 1%. This is likely partly due to genetic/hereditary variations in the immune system that predispose the patient and their family to invasive disease. It is likely as much the patient as the organism that leads to infection.

For family members, greater than 4 hours of exposure or contact with respiratory secretions antibiotic prophylaxis is recommended. And no physician has EVER spent 4 hours in a room with a patient.

In contrast, despite studies, there is no benefit to be found in treating colonized people or their contacts outside of invasive disease as nicely summed up by UpToDate:

“There are no recommendations for eradicating nasopharyngeal carriage in the community outside of an outbreak or a patient with invasive meningococcal disease. There are three problems with attempting to eliminate nasopharyngeal carriage in the community:

Spontaneous loss and acquisition of carriage are common. This was illustrated in a study in military recruits in which 34 percent experienced one or more changes in carrier status over time.

Recurrent colonization may occur after prophylaxis. In a community-wide prophylaxis program in a semi-closed kibbutz population in Israel, the colonization rate of group B meningococcus dropped from 4.6 percent at baseline to 0 percent at three weeks; it then rose to 0.5 percent at six months and 3.9 percent (similar to the baseline level) at one year.

Antimicrobial prophylaxis has no proven clinical efficacy outside of an outbreak. The meta-analysis cited above-included trials in healthy carriers. Clinical efficacy of eradication could not be assessed since there were no cases of disease following antibiotics or placebo.”

How about health care providers? There are at best a half dozen cases of secondary spread to HCWs ever reported and they all had one factor in common: exposure to respiratory secretions without proper PPE:

“Transmission of N. meningitidis to health-care personnel has occurred after unprotected exposure to infected patients during endotracheal intubation, airway suctioning, and oxygen administration (6–8), but more than one occupationally acquired infection from the same index patient has not been reported. Findings from this investigation indicate that breaches in infection control…likely contributed to secondary cases of meningococcal disease (1).”

And the first step when the issue of meningitis is raised should be to put on a mask.

Unless exposed to direct secretions, no antibiotic prophylaxis is warranted, only driving cost, toxicity, and resistance without benefit.

“To be on the safe side, any person directly exposed to the case’s nasopharyngeal secretions (e.g., through kissing or mouth-to-mouth resuscitation) is also advised to take prophylaxis. On the other hand, health care workers who haven’t had contact with secretions are not at risk and do not benefit from prophylaxis (Pubmed).”

Here is a suggested algorithm

1) Meningitis is suspected.

Droplet Isolation i.e. surgical masks. Viola. Everyone is safe.

2) LP shows meningitis by cell count, protein, glucose.

Wait. No hurry for prophylactic antibiotics, Meningococcus is not like lice, jumping off the patient on to you.

3) Gram stain is negative or has gram-negative rods or gram-positive cocci.

Meningococcus is gram-negative diplococci. Wait. It isn’t Meningococcus; prophylactic antibiotics will not be needed.

4) Gram stain has gram-negative diplococci.

Wait. No hurry.

5) Cultures grow N. meningitis.

Prophylaxis for those who were directly exposed to respiratory secretions: mouth to mouth, suctioning, intubation or other respiratory procedures without PPE.

Other health care providers do not need prophylaxis and to do so would be, and I have to be careful of the adjective I use in an official communication, let's say ill-advised.

However, everyone who has even the remotest contact with a meningococcal disease freaks out and wants prophylaxis. In a recent case I had an anesthesiologist place a line in a patient with meningococcal disease, actually followed all isolation procedures, and still thought they have an exposure that warranted the use of ciprofloxacin, What are you gonna do? It is a battle that is probably not worth fighting; I figure the ciprofloxacin is more of an anxiolytic.


There is a vaccine that covers A, C, and W-135. It's an OK vaccine; my children got it when they went off to college; it does not cover serotype B, for which a separate vaccine became available in 2015.

There are two types of meningococcal vaccines available in the United States: Meningococcal conjugate vaccines (Menactra® and Menveo®) and Serogroup B meningococcal vaccines (Bexsero® and Trumenba®).

The CDC recommendations

Meningococcal Conjugate Vaccine Recommendations Adults should get a meningococcal conjugate vaccine (Menactra® or Menveo®) if they:

  • Have a rare type of disorder (complement component deficiency)
  • Taking Eculizumab
  • Have a damaged spleen or their spleen has been removed
  • Have HIV
  • Are a microbiologist who is routinely exposed to Neisseria meningitidis
  • Are traveling to or residing in countries in which the disease is common
  • Are part of a population identified to be at increased risk because of a serogroup A, C, W, or Y meningococcal disease outbreak
  • Are not up to date with this vaccine and are a first-year college student living in a residence hall Are a military recruit Talk to your doctor to find out if, and when, you will need booster shots.

Serogroup B Meningococcal Vaccine Recommendations Adults should get a serogroup B meningococcal vaccine (Bexsero® or Trumenba®) if they:

  • Have a rare type of disorder (complement component deficiency)
  • Taking Eculizumab
  • Have a damaged spleen or their spleen has been removed
  • Are a microbiologist who is routinely exposed to Neisseria meningitidis

As of 2007, serotype X (yes X, it infects the Mac OS) is on the rise in Africa (PubMed).

For those at high risk, the vaccine should be given every 5 years: persistent complement component deficiencies (such as C3, properdin, Factor D, and late complement component deficiencies), anatomic or functional asplenia, and prolonged exposure (eg, microbiologists routinely working with Neisseria meningitidis, or travelers to or residents of countries where meningococcal disease is hyperendemic or epidemic).

N. lactamica, N. sicca, N. subflava, N. cinerea: penicillin OR a third-generation cephalosporins OR quinolones.


The meningococcal B vaccine may partially protect against GC (PubMed) and it elicits cross-reacting antibodies (PubMed).

Recurrent, and probably any, Neisseria bacteremia except gonorrhea, should raise suspicion of a terminal complement deficiency. So anyone with non-gonococcal Neisseria in their blood should get a CH50. Just do not get it during active illness as complement levels are wonky during disease.

W-135 may have a worse disease (PubMed).

What flabbers my gaster is something that should be as brain dead simple as the treatment of GC per the guidelines can't be done correctly by around 20% of providers (PubMed). While ER's and private clinics were worst, even STD clinics got it wrong 10% of the time.

As macrolide use goes up in the winter for UTI's, there is a parallel increase in GC macrolide resistance (PubMed).

Blue light kills GC (PubMed), although delivery to infected tissues can't be pleasant. And it makes me wonder just what was going on at K-Mart (PubMed),

Curious Cases

Relevant links to my Medscape blog



You Can Wait. Really. You Can.

How did THAT get THERE?

Like Birding. But Interesting.

Brave New World

Last Update: 01/03/21.