# 42 - SECTION 6 Diseases Caused by Gram-Negative Bacteria

## SECTION 6 Diseases Caused by Gram-Negative Bacteria

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PART 5
Infectious Diseases
review of the literature. Arch Surg 138:272, 2003.
Section 6	 Diseases Caused by 

Gram-Negative Bacteria
Manish Sadarangani, Andrew J. Pollard

Meningococcal 

Infections
■
■DEFINITION
Infection with Neisseria meningitidis most commonly manifests as 
asymptomatic colonization in the nasopharynx of healthy adolescents 
and adults. Invasive disease occurs rarely, usually presenting as either 
bacterial meningitis or meningococcal septicemia. Patients may also 
present with occult bacteremia, pneumonia, septic arthritis, conjuncti­
vitis, and chronic meningococcemia.
■
■ETIOLOGY AND MICROBIOLOGY
N. meningitidis is a gram-negative aerobic diplococcus that colonizes 
humans only and causes disease after transmission to a susceptible 
individual. Several related neisserial organisms have been recognized, 
including the pathogen N. gonorrhoeae and the commensals N. lactam­
ica, N. flavescens, N. mucosa, N. sicca, and N. subflava. N. meningitidis 
is a catalase- and oxidase-positive organism that utilizes glucose and 
maltose to produce acid.
Meningococci associated with invasive disease are usually encap­
sulated with polysaccharide, and the antigenic nature of the capsule 
determines an organism’s capsular group (serogroup) (Table 160-1). 

TABLE 160-1  Structure of the Polysaccharide Capsule of Common 
Disease-Causing Meningococci
MENINGOCOCCAL 
CAPSULAR GROUP
CHEMICAL STRUCTURE 
OF OLIGOSACCHARIDE
CURRENT DISEASE 
EPIDEMIOLOGY
A
2-Acetamido-2-deoxyD-mannopyranosyl 
phosphate
Epidemic disease mainly in 
sub-Saharan Africa; sporadic 
cases worldwide
B
α-2,8-Nacetylneuraminic acid
Sporadic cases worldwide; 
propensity to cause 
hyperendemic disease
C
α-2,9-O-acetylneuraminic 
acid
Small outbreaks and sporadic 
disease
Y
4-O-α-D-glucopyranosylN-acetylneuraminic acid
Sporadic disease and 
occasional small institutional 
outbreaks
W
4-O-α-Dgalactopyranosyl-Nacetylneuraminic acid
Sporadic disease; outbreaks of 
disease associated with mass 
gatherings; epidemics in subSaharan Africa
X
(α1→4) N-acetylD-glucosamine-1phosphate
Sporadic disease and large 
outbreaks in the meningitis 
belt of Africa
In total, 12 capsular groups have been identified (A–C, X–Z, E, W, 
H–J, and L), but just six of these—A, B, C, X, Y, and W (formerly 
W135)—account for the majority of cases of invasive disease. Group D 
is often listed as the thirteenth capsular group but has been identified 
as an unencapsulated variant of group C. Meningococci are commonly 
isolated from the nasopharynx in studies of carriage; the lack of capsule 
often is a result of phase variation of capsule expression, but as many as 
16% of isolates lack the genes for capsule synthesis and assembly. These 
“capsule-null” meningococci and those that express capsules other than 
A, B, C, X, Y, and W are only rarely associated with invasive disease and 
are most commonly identified in the nasopharynx of asymptomatic 
carriers.
Beneath the capsule, meningococci are surrounded by an outer 
phospholipid membrane containing lipopolysaccharide (LPS, endo­
toxin) and multiple outer-membrane proteins (Figs. 160-1 and 160-2). 
Antigenic variability in porins expressed in the outer membrane 
defines the serotype (PorB) and serosubtype (PorA) of the organ­
ism, and structural differences in LPS determine the immunotype. 
Serologic methods for typing meningococci are restricted by the 
limited availability of serologic reagents that can distinguish among 
the organisms’ highly variable surface proteins. Where available, 
high-throughput antigen gene sequencing has superseded serology for 
FIGURE 160-1  Electron micrograph of Neisseria meningitidis. Black dots are 
gold-labeled polyclonal antibodies binding surface opacity proteins. Blebs of outer 
membrane can be seen being released from the bacterial surface (arrow). (Photo 
courtesy of D. Ferguson, Oxford University.)