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Infections in patients with lupus erythematosus disseminatus.

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EDITORIAL
Infections in Patients with Lupus Erythematosus Disseminatus
Physicians caring for patients with systemic lupus erythematosus (SLE) know that
opportunistic infections occur. Sometimes
the reasons are obvious; intravenous or
bladder catheters or other violations of an
intact integument are frequently seen in
hospitals and are common sources of o p
portunistic infection in hospitalized patients. Less obvious are the effects that SLE
lung or renal disease may have on that
organ’s immune mechanisms. Certainly it
seems probable that a restricted lung that
does not clear secretions will be readily
infected and underlying renal disease, for
unidentified reasons, does appear to make
the kidney more susceptible to infection.
Poor blood perfusion due to vasculiltis decreases the delivery of the last line of host
defenses, the immune cells, specifically
polymorphonuclear neutrophils, monocytes,
and macrophages, and lymphocytes, along
with humoral factors such as opsonins and
com plemen t. Lymphocytes recently have
been divided into T or theta lymphocytes
responsible for mononuclear cell immunity
(delayed hypersensitivity or transplantation
immunity), and B or beta lymphocytes reponsible for the production of immunoglobulins. Through studies of patients with
certain neoplastic diseases or with congenital immune deficiency syndromes it has
become apparent that certain microorganisms have a predilection for individuals
with specific deficiencies. If one knows the
specific deficiency or the underlying disease,
one can predict the type of infection that
will be seen in a particular host. For instance we have learned that meningitis in
a patient with Hodgkin’s Disease and a
normal neutrophil count will almost surely
be due to Listeria monocytogenes or Cryptococcus neoformans. In contrast meningitis in a patient with acute leukemia and
neutropenia is more likely caused by an
aerobic, enteric, gram-negative rod. T h e
patient with decreased or poorly functioning neutrophils becomes subject to infections with common pathogens such as
strepococcus pyogenes, Streptococcus pneumoniae, Staphylococcus aureus and the less
pathogenic aerobic, enteric bacilli. T h e patient with decreased or poorly functioning
T-lymphocytes or monocytes becomes prey
to organisms that are facultative intracellular parasites. These are frequently endogenous or latent infections which become
activated when the host is immunosup
pressed. T h e opportunistic bacteria or fungi in this case include L monocytdgenes,
Nocardia asteroides, Myobacterium tuberculosis, Salmonella species, C neoformans,
Histoplasma capsulatum and Coccidioides
immitis. T h e parasites and viruses include
Toxoplasma gondii, Pneumocystis carnii,
Strongyloides stercoralis, herpes simplex,
varicella-zoster, cytomegalovirus and measles. One cannot only predict what type of
infection to expect according to the type of
immunologic deficit, but the converse is
true-repeated,
severe or disseminated in-
Arthritis and Rheumatism, Vol. 17, No. 3 (MayJune 1974)
285
ARMSTRONG
fections with either of the group of microorganisms listed above would suggest either
a neutrophil or mononuclear cell defect
which might not otherwise be suspected. In
chronic granulomatous disease of childhood, a congenital immune deficiency syndrome in which the neutrophils cannot
produce hydrogen peroxide to kill engulfed
bacteria, the diagnosis is first suggested by
the fact that repeated, severe bacterial infections occur, not with all the bacteria
outlined above as invading in the presence
of neutrophil defects, but only those which
produce their own hydrogen peroxide and
do not degrade it. The pattern of repeated
severe infections with catalase-producing
bacteria almost clinches the diagnosis of
chronic granulomatous disease of childhood. This diagnosis is finally established
by in vitro tests of neutrophil engulfment
and killing.
The paper by Staples, Gerding, Decker
and Gordon (ARTHRITIS RHEUM 17: 1-10,
1974) can be looked at from this point of
view and some conclusions drawn. Carefully recorded infections in their SLE
patients over the years suggest that the
main immunologic defect is in neutrophil
function. There is only one infection with
a facultative intracellular parasite in the
patient with miliary tuberculosis. Candida
albicans infects individuals with both neutrophil or mononuclear cell defects so that
this tells us little. The organisms most commonly infecting the patients are grampositive coccal pathogens and gram-negative
enteric bacilli, so that the defect in the
patients studied was mainly in the neutro-
286
phi1 itself or in humoral factors that promote phagocytosis, such as opsonizing antibody or complement. Low nitroblue tetrazolium activity as well as faulty chemotaxis
has been demonstrated in neutrophils of
patients with SLE, and it is easy to speculate that defective complement activity is a
factor in the increased incidence of infection. What is now necessary is to document
exactly where the defect(s) lie in prospective studies measuring as many immune
parameters as accurately as possible. Although only one case appeared in this
study, we know from a number of case
reports that patients with SLE do suffer
from severe infections with facultative intracellular parasites. We can anticipate infection in these patients with this group of
organisms in the future, and studies must
include an evaluation of mononuclear cell
defenses along with their humoral factors
as well as neutrophils. It is only after we
carefully delineate the defects and tletermine their cause-eg, the basic disease or
our immunosuppressive therapy-that we
can alter our forms of therapy or consider
appropriate immunotherapy or immunoprophylaxis. In the meantime we must follow one of the main conclusions of the
authors that fever in patents with SLE is
due to lifethreatening infection until proven
otherwise.
DONALD ARMSTRONG, MD
Memorial Slonn-Kettering
Cancer Center
New York, New York
Arthritis and Rheumatism, Vol. 17, No. 3 (May-June 1974)
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