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Neisseria
German physician A. L. S. Neisser, who originally described the organism response for gonorrhea
Albert Ludwig Sigesmund Neisser was born as the son of a well known Jewish physician, Moritz Neisser. Neisser began his medical studies in Breslau in 1872. Neisser originally planned to become a specialist in internal medicine, but there was no opening for assistants in Biermer's clinic. It was therefore purely by chance that he turned to dermatology and became an assistant physician to in the dermatology clinic originally founded by Heinrich Koebner. He worked here for two years, and it was here, in 1879, Neisser discovered the gonococcus.
Neisser's discovery occurred in the wake of the rapid development of the new field of bacteriology. It was made possible in large part by his close association with Ferdinand Cohn, the botanist who also gave invaluable help to Robert Koch. Cohn taught him Koch's smear tests for the identification of bacteria. He at first called the microorganism that he thus observed "micrococcus"; they were then given the name "gonococcus" by Paul Ehrlich. Although his discovery was extremely important, it was not until the advent of penicillin that this widespread disease could be controlled. His students called him the "father of gonococcus".
Neisseria meningitidis
Other species normally colonize mucosal surfaces of oropharynx and nasopharynx and occasionally anogenital mucosal membranes. These species have limited virulence and generally produce disease only in compromised patients.
Neisseria
N. gonorrhoeae (gonococcus): gonorrhea N. meningitidis: meningitis
N. gonorrhoeae (Gonococcus)
Antigenic structure
1. Pili: enhancing attachment to host cells and resistance to phagocytosis; antigenically different among strains, and a single strain can make many antigenically distinct forms of pilin. 2. Por proteins: form porins and mediate resistance to neutrophil and serum killing. 3. Opa: associated with opaque colonies; an outer membrane protein functioning in attachment to host cells. 4. Rmp: stimulates antibodies that block serum bactericidal activity. 5. Lipooligosaccharide (LOS): lacking long-antigenic side chains; endotoxic.
6. Other proteins.
N. gonorrhoeae is capable of changing its surface antigens (particularly pilin) rapidly to avoid host defenses.
Lipopolysaccharide (LPS)
is also called endotoxin. LPS is composed of lipid A, core polysaccharide, and O-specific polysaccharide.
Lipid A anchors LPS in the lipid bilayer. It causes symptoms associated with endotoxin.
O-specific polysaccharide can be used to identify certain species and strains.
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Pathogenesis
Attachment to mucosal cells (requires pili) Invade into the cells and multiply (Opa mediates tighter association with and invasion of host cells; Por inhibits phagolysosome fusion) Pass through the cells into the subepithelial space Establish infection (LOS stimulates inflammatory response; Rmp blocks bactericidal activity)
Epidemiology
Gonorrhea occurs only in humans. Gonorrhea is transmitted by sexual contact, often by women and men with asymptomatic infections. Women have a 50% risk of acquiring the infection with a single exposure to an infected man while men have a 20% risk in the same situation. 95% infected men and 50% infected women have acute symptoms. So, asymptomatic carriage is more common in women than in men.
Rectal and pharyngeal infections are more commonly asymptomatic than genital infections.
Symptoms
1. Male: urethritis with yellow, creamy pus and painful urination. The process may extend to the epididymis (). As suppuration subsides in untreated infection, fibrosis occurs, sometimes leading to urethral strictures (sterility).
2. Female: infection starts from the endocervix () , and results in vagina discharge, dysuria () , and abdominal pain. Uterine tubes may be involved, causing salpingitis (), fibrosis, and obliteration of the tubes (20% may become infertile). When gonococcal cervicitis is either asymptomatic or unrecognized, the patient may progress to pelvic inflammatory disease (PID).
bilateral conjunctivitis often follows vaginal delivery from an infected mother. The symptoms are eye pain, redness, and a purulent discharge. The organism can cause permanent injury to the eye in a very short time; prompt recognition and treatment are essential to avoid blindness. prevention: 1% tetracycline, 0.5% erythromycin or 1% silver nitrate eye ointment.
4. Gonococcal bacteremia (1-3% of infected women and much lower percent of infected men) can lead to fever, pustular () rash over the extremities, tenosynovitis ( ) and suppurative arthritis.
gonorrhea
Immunity
Repeated gonococcal infections are common, because protective immunity to reinfection does not develop due to the antigenic variation of gonococci. This makes development of effective vaccines difficult.
Treatments
Resistance to penicillin G (PPNG: penicillinase-producing N. gonorrhoeae) and tetracycline is common. Resistance to fluoroquinolones has also become prevalent.
Laboratory Diagnosis
Gram stain (gram-negative diplococci in PMNs): Sensitive (>90%) and specific (98%) for men with purulent urethritis. Less sensitive for asymptomatic men (<60%). Relatively insensitive for both symptomatic and asymptomatic women. Culture: Avoid drying of specimen (genital or rectal) and low temperature. Direct inoculation of specimens onto prewarmed media is preferred. Inoculate both the selective media (e.g., modified ThayerMartin) and non-selective media (e.g., chocolate blood agar; for strains that are sensitive to vancomycin).
Identification
N. gonorrhoeae is distinguished from other species by acid production from oxidation of glucose, but not from other sugars. Direct detection of N. gonorrhoeae in clinical specimens by PCR with specific primers.
Neisseria meningitidis
(meningococcus)
Antigenic structure
1. Capsular polysaccharide: more than 13 serogroups have been identified (serogroups A, B, C, X, Y, and W135 are most commonly isolated). 2. Pili (allow bacterial colonization of nasopharynx). 3. Outer membrane proteins: these are analogues to the Por and Opa proteins of gonococci. 4. Lipooligosaccharide (LOS): responsible for diffuse vascular damage in meningococcal infections.
Fulminant meningococcemia
High fever and hemmorrhagic rash.
There may be disseminated intravascular coagulation ( ) with shock, and circulatory collapse (Waterhouse-Friderichsen syndrome: bilateral destruction of adrenal gland.) Meningitis is the most common complication of meningococcemia.
A milder septicemia with low-grade fever, arthritis, and petechial skin lesions that persist for days or weeks may be observed.
Other syndromes: pneumonia, arthritis, and urethritis.
Meningococcemia can be prevented by specific bactericidal antibodies in serum.
Meningitis
Symptoms: begins suddenly, with intense headache, vomiting, and stiff neck, and progress to coma within a few hours. Mortality: nearly 100% if untreated; <10% in patients treated promptly with appropriate antibiotics.
Immunity
Protective immunity is the group- or type-specific, complement-dependent, bactericidal antibodies. Serogroup B, whose capsule contains sialic acid, is relatively nonimmunogenic.
Laboratory Diagnosis
Specimen: blood and cerebrospinal fluid (CSF). >107 bacteria/ml of CSF are normally found in untreated patients. Gram stain: gram-negative diplococci in PMNs. Culture: alternative blood culture methods are required because additives in the blood culture broths can be toxic for this organism. Identification: acid formation with glucose and maltose, but not others.
Treatment
Penicillin G is the drug of choice.
Areas with frequent epidemics of meningococcal disease. This is known as the Meningitis Belt of Africa, and visitors to these locales may benefit from meningitis vaccine. Large-scale outbreaks rates as high as 400-500 cases per 100,000 population (compared to 1-2 cases per 100,000 population in USA). Menigitis
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