Gram (-) Cocci Flashcards
List the gram(-) cocci
Neisseria meningitides
Neisseria gonorrheae
What do Neisseria species look like?
Gram(-) diplococci
What are the culture requirements for Neisseria species?
Chocolate agar - cannot grow on blood bc they are inhibited by some lipids/elements of the blood agar. If you heat up blood agar you get chocolate agar (the inhibitors are inactivated)
VPN (Thayer Martin) agar - enriched with Vancomycin, Polymyxin, Nystatin
Who is at increased risk of infection via Neisseria species?
People with C5-C9 Complement deficiency - they cannot form MAC complexes
What are the 2 main virulence factors shared by Neisseria species?
Pillus (fimbrae) - allows them to attach to mucosal surfaces. Also allows frequent genetic rearrangement. Pilli display antigenic variation making it hard for our Immune System to target it. Also prevents a lasting immune response.
IgA Protease - cleaves IgA at its hinge point facilitating survival along mucosal surfaces
What facilitates spread of Neisseria meningitidis?
Close quarters (college dorms)
How is N. meningitidis transmitted?
respiratory droplets (sneezing, coughing, kissing, sharing drinks, simple close contact)
What is unique about N. meningitidis’ biochemistry compared with N. gon?
N. meningitidis ferments maltose.
What does N. meningitidis colonize first?
nasopharynx (respiratory droplets)
What is N. meningitidis’ capsule made out of?
polysaccharides
The capsule inhibits phagocytosis (important virulence factor).
N. meningitidis vaccine
contains polysaccharide capsule
Does NOT contain Type B capsule - most infections in US and other developed countries are by the Type B strain
N. meningitidis course through body
Colonizes nasopharynx. Establishes infection by invading through the blood. In the blood, it leads to a huge inflammatory response which is generated by lipooligosaccharides (LOS proteins). These envelope proteins are Neisseria’s version of LPS. It grows so much LOS that the proteins end up outgrowing the bacteria and begin falling off. It is these pieces of fallen off LOS envelope that cause the inflammatory response.
The first step of pathogenesis is the inflammatory response. This leads to increased permeability of capillaries and leakage of fluid into extravascular space. This leads to hypovolemia.
You get a characteristic petecheal rash indicative of thrombocytopenia. The petecheae can progress to purpura and echymoses which is a sign that the illness is progressing to DIC (Disseminated Intravascular Coagulation).
If it progresses to DIC you’d see oozing at venipuncture sites or bleeding gums.
Think N. meningitidis is pt has meningitis + this rash.
What causes shock in patients with N. meningitidis?
Capillary leakage from hypovolemia.
Waterhouse-Friderichsen Syndrome
Characterized by hemorrhage of adrenals
N. meningitidis
As pt becomes hypovolemic, peripheral vasoconstriction maxes out to try to maintain BP. When this happens, adrenals can become poorly profused and infarct.
Resulting adrenal insufficiency can further contribute to shock and is often fatal.
Overall mortality rate for pts with N. meningitidis
15% even with antibiotics
Early treatment is important and improves outcomes.
Tx for meningiococcal meningitis
3rd gen cephalosporin (Cephtriaxone)
Give close contacts prophylaxis with Rifampin bc it spreads so easily in close contact.
Close contact is someone who has spent more than 8hrs with a patient during the 7 days prior to onset.
N. gonorrheae respiration
Facultative intracellular - likes to invade PMNs
What is the most common initial infection site for N. gonorrheae?
genitalia in men and women
Which Neisseria species are sickle cell patients more susceptible to?
Meningitidis (it is encapsulated)
How does N. gonorrheae present in men?
Urethritis
It can travel up the tract and cause prostatitis or orchitis
Characteristic white, purulent discharge (thicker and more purulent than in chlamydia)
Can also cause polyarthritis that is asymmetric (esp in knee)
Joint tap will show purulent synovial fluid that doesn’t gram stain (infection is intracellular)
How does N. gonorrheae present in women?
Urethritis
Characteristic white, purulent discharge (thicker and more purulent than in chlamydia)
Can also cause polyarthritis that is asymmetric (esp in knee)
Joint tap will show purulent synovial fluid that doesn’t gram stain (infection is intracellular)
When infection ascends in women, it can cause Pelvic Inflammatory Disease. PID can cause scarring that could lead to infertility or ectopic pregnancies
PID can also spread to peritoneum. This is Fitz Hugh Curtis Syndrome. This leads to adhesions that form to capsule of liver. Long/thin adhesions are called violin-string adhesions.
Fitz Hugh Curtis Syndrome
Pelvic Inflammatory Disease that has spread to peritoneum. This leads to adhesions that form to capsule of liver. Long/thin adhesions are called violin-string adhesions.
Congenital infection by N. gonorheae
If an expecting mother has an untreated gonococcal infection, she can pass it on to baby during delivery
Manifests as purulent conjunctivitis that occurs within first week 5 days of life (Chlamydia does this too, but like a week later). Remember this EARLY ONSET.
Tx for N.gonorrheae
Cephtriaxone
This is all you need, but it is not the whole answer.
There is a high chance that a patient who has gonorrhea also has chlamydia.
Assume that the patient has a coinfection and treat for chlamydia too (same for treating the neonatal conjunctivitis too).
Treat the Chlamydia with a macrolide (azithromycin) or doxycycline.
Summary: Tx for gonorrhea is Cephtriaxone + azithromycin/doxycycline
