[PAGID] Malakoplakia

[John Ziegler]

-

I'll append a message I received from a colleague on this topic. John
Ziegler

From: pagid-bounces at list.clinimmsoc.org
[mailto:pagid-bounces at list.clinimmsoc.org] On Behalf Of Anita Gewurz
Sent: Wednesday, 27 February 2008 10:18 AM
To: pagid at list.clinimmsoc.org
Subject: [PAGID] Malakoplakia

Dear Colleagues: 
We have a 30-year-old African-American female patient who has been diagnosed
with colonic and renal malakoplakia (variant spelling, malacoplakia). This
is a very rare 
... 
worsening, and the prognosis is death from obstruction or other
complications. Our questions are do you have any advice for treating or
testing this patient? 
Thank you. 
Sincerely, 
Lily Hwang MD, A/I Fellow-in-Training 
Anita Gewurz MD <agewurz at rush.edu> 

From: a.lloyd at unsw.edu.au [mailto:a.lloyd at unsw.edu.au] 
Sent: Thursday, 4 May 2006 5:52 PM
To: Philip.Jones at unsw.edu.au; j.ziegler at unsw.edu.au
Cc: Matthew Watts; Lisa Elliott
Subject: Malakoplakia


Dear Phil, John, Matt, 
Actually there is a fair bit written about this "malacoplakia" beast please
see article below - unfortunately pdf not available - most articles are
antique. The underlying immunological defect remains unclear, but appreas
clearly to involve defective killing of Gram negatives especailly E coli
within macrophages. It occurs in both children and adults and is associated
strongly with immunodeficiency (esp steroid use). I am unsure whether it is
worth exploring antigen-driven interferon-gamma production, as it is not
likely to be a T cell defect. What may be of greater interest is to test in
vitro whether there is a killing defect and then to see if gamma interferon
added in vitro (or TNF) would restore the killing capacity. The killing
assay would require expertise a little outside my realm as it wuld have to
be done with a colony forming units-type assay after incubation of a
designated number of E coli with a mononuclear cell prep. We can easily
separate and store serum and PBMC with a view to this assay, but I wonder
whether there is a person who would like a small
immunological/microbiological lab project to set up the assay and then study
the bloods from this guy now and again in a month or so - Matt? or would
Brynn be interested John?? 
Ultimately, this would only be a worthwhile endeavour if it were publishable
as a case report plus lab studies... 

Input into the discussion welcome..... 


Regards,
Andrew

Professor Andrew Lloyd AM, MBBS, MD, FRACP.

Ph: (02) 9385 2534
Ph (mobile): 0413 112 701
Fax: (02) 9385 1514
Email: A.Lloyd at unsw.edu.au

UNIVERSITY:
Inflammatory Diseases Research Unit,
School of Medical Sciences,
University of New South Wales,
Sydney, NSW 2052 Australia

HOSPITAL:
Department of Infectious Diseases,
Prince of Wales Hospital,
Barker St, Randwick NSW 2031 

Volume 156(5), 11 March 1996, pp 577-583

Malacoplakia: Two Case Reports and a Comparison of Treatment Modalities
Based on
a Literature Review
[Clinical Observation]

van der Voort, Peter H. J. MD; ten Velden, Jos J. A. M. MD; Wassenaar,
Ronald
P. MD; Silberbusch, Joseph PhD, MD

----------------------------------------------

Outline

Abstract

REPORT OF CASES

CASE 1

CASE 2

COMMENT

PATHOGENESIS

REVIEW AND TREATMENT STRATEGIES

CONCLUSIONS

REFERENCES

Graphics

Figure 1
Figure 2
Figure 3
Table 1
Table 2

Abstract

Malacoplakia is a rare infectious disease that has been almost exclusively
reported in urology and pathology journals. We studied two cases of
malacoplakia
that were primarily referred to the department of internal medicine because
of
fever and abdominal masses. In one patient, malacoplakia was diagnosed in
the
unusual ovarian location, while in the other patient a large renal mass was
found and ciprofloxacin therapy failed because of bacterial resistance. The
clinical and radiologic appearance of malacoplakia often mimics that of a
malignant tumor. The principal disorder is probably a monocytic-macrophagic
bactericidal defect. A definitive diagnosis depends on microscopic detection
of
Michaelis-Gutmann bodies by means of von Kossa stain. We outlined treatment
strategies on the basis of a review of the literature since 1981, which
included
140 cases. If possible, immunosuppressive drugs should be stopped. Quinolone
antibiotic treatment and surgical excision or incision and drainage lead to
the
highest cure rates (90% and 81%, respectively). Specific intracellular
penetration of quinolone antibiotics is a possible reason for the higher
cure
rate achieved with these antibiotics. Bethanechol has been suggested to
correct
the supposed fundamental disturbance by increasing the intracellular cyclic
guanosine monophosphate concentration, but there is still no convincing
evidence
of its clinical efficacy.

(Arch Intern Med. 1996;156:577-583)

----------------------------------------------

Malacoplakia is a rare chronic inflammatory process usually caused by
Escherichia
coli and most commonly affecting the urinary tract. Microscopically, a
xanthogranulomatous inflammation with an abundance of foamy macrophages
containing the pathognomonic Michaelis-Gutmann bodies can be seen. The
clinical
appearance is a mass lesion that is difficult to distinguish from a
neoplasm.
Long-term antibiotic treatment is usually not effective, but recently it has
been suggested that ciprofloxacin, an intracellular penetrating drug, might
cure
even extensive malacoplakia [1]

We will report two cases of malacoplakia, distinguished by an unusual
location
in one and failure of intensive ciprofloxacin treatment in the other. No
trials
have been conducted to compare treatment efficacy. By reviewing the
literature
since 1981, we were able to outline treatment recommendations.

REPORT OF CASES

CASE 1

A 37-year-old woman from Ghana had had five immature parturitions between
1978
and 1982. An operation had been performed in Ghana to reconstruct a uterus
bicornis. In 1988 she moved to the Netherlands. Two years later she was
admitted
to another hospital because of fever and acute renal failure. Blood cultures
yielded E coli. The focus of the E coli sepsis was not determined, although
a
nonfunctioning hypoplastic left kidney was found. In addition a hepatitis C
infection, sickle cell trait and iron deficiency anemia were found.

Sixteen months later, the patient was admitted to our hospital because of
tiredness and weight loss. She had a fever with rigors but without abdominal
complaints. On physical examination she was anemic and moderately ill, with
a
temperature of 39.2 degrees C. A left-sided, nonpainful, lower abdominal
mass
was palpable. The white blood cell count was 13.0x109/L; creatinine level
was 69
micromole/L (0.9 mg/dL). Results of urinalysis were unremarkable and urine
culture was sterile, but E coli grew from multiple blood cultures. Computed
tomography showed a mass on the left side of the uterus (Figure 1). Gallium
scintigraphy showed activity in this mass, suggesting an abscess of the left
adnexa, without activity in the hypoplastic left kidney.

----------------------------------------------



Figure 1. Computed tomographic scan after intravenous administration of
contrast material. A large inhomogeneous mass with internal septa and
peripheral
enhancement is demonstrated in the pelvis (open arrows). The mass contains
the
left ovary and seems continuous with the uterus (solid arrow)



----------------------------------------------

The patient was treated with cefuroxime sodium. Her temperature decreased,
but
fever recurred and E coli was again cultured from her blood after the drug
was
discontinued. Through laparotomy, a 10-cm adnexal tumor with well-defined
margins but in close relation to the uterus was removed. On histopathologic
examination, it appeared to be an inflammation of the left ovary that
consisted
mainly of foamy macrophages (xanthogranulomatous inflammation) with
intracytoplasmatic
calcium-containing inclusion bodies (Figure 2). These Michaelis-Gutmann
bodies
were diagnostic of malacoplakia. Culture of resected tissue disclosed the
same
strain of E coli as was previously found in the blood. Postoperatively, the
patient made a full and lasting recovery.

----------------------------------------------



Figure 2. Resected ovary with xanthogranulomatous inflammation, containing
Michaelis-Gutmann bodies (round, black intracytoplasmatic dots) (von
Kossa's,
x400)



----------------------------------------------

CASE 2

A 68-year-old man was admitted to the hospital because of fever, weakness,
weight loss, and night sweats. He was using sulfamethoxazole-trimethoprim
because of recurrent urinary tract infections. Results of a previous
evaluation
of the lower urogenital tract had been unremarkable. On physical
examination, he
had a temperature of 38.6 degrees C, a nonpainful mass in the left upper
part of
the abdomen, and a slight weakness in the left leg.

The white blood cell count was 11.0x109/L, with a strong shift to the left
in
the differential cell count. The erythrocyte sedimentation rate was 42 mm/h;
hemoglobin and creatinine levels were normal. Escherichia coli resistant to
sulfamethoxazole-trimethoprim and nalidixic acid grew from cultures of the
urine. Treatment with amoxicillin-clavulanic acid had no effect on the
temperature, and the erythrocyte sedimentation rate and leukocytosis
increased.
Computed tomography (Figure 3) showed a 9-cm, solid mass in the lower part
of
the left kidney with invasion of the psoas musculature, raising suspicion of
renal carcinoma. Fine-needle aspiration showed growth of the same strain of
E
coli. Biopsy showed a xanthogranulomatous inflammation with
Michaelis-Gutmann
bodies, leading to the diagnosis of malacoplakia.

----------------------------------------------



Figure 3. Computed tomographic scan after intravenous administration of
contrast material. The left kidney is displaced ventrally by a large
necrotic
mass with peripheral enhancement. The mass is continuous with the lower pole
of
the kidney and invades the left psoas musculature (solid arrow) and
posterior
abdominal wall (open arrow)



----------------------------------------------

Therapy was changed to ciprofloxacin hydrochloride, 500 mg twice daily. The
fever initially disappeared and ciprofloxacin treatment was continued on an
outpatient basis. Within 2 weeks he was readmitted in a severely
deteriorated
state with high temperatures and a remarkable increase of the palpable mass.
Necrotic tissue was drained through surgical incision. Escherichia coli,
resistant to ciprofloxacin, was isolated from this material, and the use of
this
antibiotic was discontinued. Rapid improvement occurred in the weeks
thereafter.
The mass decreased in size, and temperature and laboratory values became
normal.
Computed tomography after 4 weeks showed a slight thickening of the
perirenal
tissue. Six months later, no symptoms remained and ultrasonography showed
normal
kidneys.

COMMENT

Malacoplakia is an uncommon chronic infection with distinctive histologic
features. At least 40% of the cases have been found by autopsy or by routine
histopathologic examination of resected tissues, reflecting the difficulty
of
diagnosing this disease clinically. This feature also results from the low
incidence of the disease, as well as a wide spectrum of clinical
presentations.

In the urinary tract, which is frequently affected, hematuria and recurrent
urinary tract infections are the most consistent findings. Other symptoms
may be
caused by obstruction of the urinary or gastrointestinal tract when the mass
lesion expands in time. The more extensive lesions can cause tiredness,
weight
loss, fever, and night sweats. Palpable masses can be found. The erythrocyte
sedimentation rate is increased, anemia may be severe, and leukocytosis is
common. The lesions are detectable by gallium scintigraphy [2-6], which may
be
an important method to determine the exact location. Computed tomography
often
shows inhomogeneous masses with necrosis [7-9]. The lesions contain
bacteria, in
particular E coli, which can be found in urine when the lesions communicate
with
the urinary tract. Positive blood cultures, as in our first case, are rarely
found.

The first pathologic description was given by Michaelis and Gutmann [10] in
1902, followed by von Hansemann [11] in 1903, who introduced the term
malacoplakia.
The macroscopic appearance is usually a yellowish brown, solid, soft mass,
not
unlike that of a carcinoma. Foamy macrophages or histiocytes, together with
other inflammatory cells, form a dense infiltration known as
"xanthogranulomatous
inflammation." Pathognomonic intracytoplasmic inclusion bodies must be
present
to make a definite diagnosis. These Michaelis-Gutmann bodies contain calcium
and
can best be seen with von Kossa stain.

Electron microscopic studies [12] of the histiocytes show phagolysosomes
containing bacteria in various states of disintegration. The ultimate stage
consists of the formation of the 4-to 10-microns Michaelis-Gutmann bodies,
which
are calcified mucopolysaccharides and lipids of similar composition as in
the
bacterial cell wall, especially E coli, strongly suggesting the bacterial
origin
of these particles.

PATHOGENESIS

Only a few investigators have addressed the question of pathogenesis. The
consistent finding of E coli strongly suggests a causative role. Although
most
authors agree that a diminished capacity of macrophages for lysis of
bacteria is
the basic disturbance [13-16], the molecular defect remains to be
determined.

An immunodeficient state seems to favor the development of malacoplakia,
since
16 cases have been reported in these patients [2,14,17-29], 11 of whom used
prednisone for autoimmune disease. Three had hypogammaglobulinemia
[23,24,27],
one had IgA deficiency [26], and one had acquired immunodeficiency syndrome
[28]. In addition, there are reports of 12 renal transplant recipients who
used
prednisone and azathioprine [14,30-39]. However, the malacoplakia was not
always
located in the transplant itself. Biggar et al [14] found diminished
leukocyte
killing function for E coli and Staphylococcus aureus in four patients who
returned to normal after discontinuing the immunosuppressive drugs.

Virtually all pathogenetic studies have focused on intracellular cyclic
nucleotide levels of macrophages. The most thorough study was done by Abdou
et
al [13]. Similar to findings in the Chediak-Higashi syndrome, they found a
decreased intracellular concentration of cyclic guanosine monophosphate
(cGMP)
in the macrophages of one patient with malacoplakia and
hypogammaglobulinemia.
This could lead to a decreased fusion of primary lysosomes with phagosomes
containing bacterial products, resulting in incomplete bacterial killing and
the
formation of Michaelis-Gutmann bodies. Abdou et al also showed an increase
in
the intracellular cGMP concentration and bactericidal activity of blood
monocytes when bethanechol chloride was added to the cell culture, or when
the
patient was pretreated with bethanechol. In contrast, Webb et al [24] did
not
find decreased cGMP levels in their hypogammaglobulinemic patient with
malacoplakia. Wener et al [20] did find a decreased cGMP level in their
patient
who used prednisone, but incubation with bethanechol failed to give a
substantial
increase. Biggar et al [14] found decreased bacterial killing but normal
cyclic
adenosine monophosphate (cAMP) and cGMP levels in patients with
malacoplakia.
The bactericidal effect did not improve after carbachol treatment.

Both Wener et al [20] and Curran [40] proposed that a diminished cGMP/cAMP
ratio
might be more important than lowered cGMP level per se. Ascorbic acid might
be
able to correct this ratio, as it increases cGMP level in normal monocytes
[41]
and decreases cAMP level in monocytes of patients with the Chediak-Higashi
syndrome [42]. It has been used in treatment of malacoplakia, but effects on
monocyte function have not been measured.

These partly conflicting results still do not give a better understanding of
the
bactericidal defects of the host macrophages and cast some doubts on the
role of
cGMP and cAMP.

REVIEW AND TREATMENT STRATEGIES

Using MEDLINE, we were able to collect from 1981 to 1993 140 case reports of
malacoplakia with 143 locations [1-6,8,9,14,17-40,43-115]. In the
non-English
literature, 62 case reports were found. Stanton and Maxted [7] reviewed 153
of
200 cases up to 1981. Thus, the total number of reported cases is
approximately
400.

We reviewed the English literature since 1981 and summarized the
characteristics
of these 143 locations (Table 1). The majority of reported locations (70%)
involved the urinary tract (Table 1), but virtually every organ can be
affected.
The ovarian location, as in our first case, was reported only once before,
although a location in the testes and epididymides in men were reported more
often. Men and women were equally affected (49% and 51%, respectively), but
in
women the urinary tract was more often involved. In 38 cases no data on
bacterial culture were available. In 20 of 105 cultures, no microorganisms
were
found, possibly because of previous antibiotic treatment. Of the remaining
85
cultures, 82 (96%) contained E coli.

----------------------------------------------



Table 1. Characteristics of 143 Localizations of Malacoplakia



----------------------------------------------

(Table 2) gives the outcome for 122 of 143 locations according to treatment
modality. For the other 21 cases, outcome was not reported. In many smaller
lesions, for instance in the male and female genital tract, diagnosis was
made
after resection. In larger lesions, surgical intervention usually consisted
of
incision and drainage. Most of these latter cases were concomitantly treated
with various antibiotics. The cure rate in 59 cases with any surgical
intervention
was 81%.

----------------------------------------------



Table 2. Cure Rates of Different Treatment Modalities in 122 Cases With
Known Outcome



----------------------------------------------

Twenty-nine cases were treated with antibiotics alone. Four (21%) of 19
patients
were cured by nonquinolone antibiotics, all sulfamethoxazole-trimethoprim
[3,43,88]

Failures of this antibiotic therapy have also been reported [27,54,61,70].
Amoxicillin or ampicillin [4,61,71,110], cephalosporins [5,38], and
aminoglycosides
[61,92] were unsuccessful. Seven of eight patients were cured with
ciprofloxacin
(500 to 1500 mg daily) without concomitant surgery [1,4,27,61,72]. In the
other
case [55], a substantial response but no complete cure was achieved. Of two
known cases treated with ofloxacin, one had a temporary response and one was
unavailable for follow-up. Norfloxacin was successful once [113]. The
ciprofloxacin
failure in our second case could have resulted from a preexisting resistance
to
nalidixic acid, which is known to evolve easily into ciprofloxacin
resistance.
The higher effectiveness (cure rate, 90%) of quinolone antibiotics and
sulfamethoxazole-trimethoprim is probably the result of their ability to
penetrate and concentrate in macrophages [116-118]

As discussed above, bethanechol, a choline agonist, might correct the
altered
cGMP level in macrophages. One of four reported cases treated with
bethanechol
alone was cured [24]. The hypogammaglobulinemia in this patient might
represent
a distinct situation in which bethanechol is a useful drug [13]. One other
patient with hypogammaglobulinemia was cured with bethanechol and
ciprofloxacin
[27]. Three of eight patients with relatively small lesions were cured by
treatment with both bethanechol and nonquinolone antibiotics [26,30,56]. The
combination of sulfamethoxazole-trimethoprim with both bethanechol and
ascorbic
acid was successful twice [6,57]

Eleven renal transplant recipients were treated by dose reduction or
discontinuation
of azathioprine and prednisone. This led to cure in 10 of them and a partial
response in the 11th patient [14,30,31-39]. In contrast, 11 patients who
used
prednisone for autoimmune disease and continued this medication had a
variable
outcome [2,14,17-22,25]. One report claimed successful treatment with
prednisone
and azathioprine for renal malacoplakia in an 8-week-old infant after
unsuccessful
treatment with antibiotics. The mechanism involved was thought to be
reduction
of ongoing release of cytokines, but the report lacked laboratory
investigations
[44]

Five (83%) of six untreated patients died. Overall, mortality was 15%
(18/123).
The highest mortality rate, 22%, was found for upper urinary tract locations
(kidney and ureter). A review of all known cases of bilateral kidney
malacoplakia
showed an 80% mortality rate for antibiotics without intracellular activity
and
22% in cases of intracellular penetrating antibiotics, such as quinolones
and
sulfamethoxazole-trimethoprim [45]

According to the analysis of the 140 case reports, treatment could be
instituted
along the following steps: (1) If feasible, stop prednisone and azathioprine
treatment in those cases where malacoplakia developed during the use of this
medication. (2) Perform surgical resection and drainage in combination with
ciprofloxacin administration. (3) If surgery is impossible, give
ciprofloxacin
hydrochloride, 500 mg twice daily. (4) Whether the addition of bethanechol
and
ascorbic acid offers any advantage to the other treatment modalities remains
to
be proved.

CONCLUSIONS

In malacoplakia, defective bacterial killing by macrophages leads to chronic
xanthogranulomatous disease. In the vast majority of cases, E coli is the
causative microorganism. The exact molecular defect has yet to be
determined. By
reviewing 140 case reports, we outlined treatment strategies to be used by
clinicians confronted with this disease.

Surgical excision or incision and drainage together with quinolone
antibiotics
seems to be the most effective treatment. Discontinuation of
immunosuppressive
drugs is also associated with cure of malacoplakia.

Accepted for publication August 25, 1995.

We thank P. J. G. M. Rietra, MD, PhD, for his valuable comments.

Reprint requests to Department of Internal Medicine, Onze Lieve Vrouwe
Gasthuis,
PO Box 95500, 1090 HM Amsterdam, the Netherlands (Dr van der Voort).

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