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JNEPHROL 2010 ; 23 ( 06 ) : 732 - 737


Urinary balantidiasis: diagnosis at a glance

by urine sediment examination
Alberto Maino1, Giuseppe Garigali2,
Romualdo Grande3, Piergiorgio Messa2,
Giovanni B. Fogazzi2

A 56-year-old Caucasian man with non-Hodgkins lymphoma, who had previously been treated with prolonged
intensive chemotherapy, was hospitalized for an acute
and reversible kidney injury of multifactorial origin.
The urinary sediment examination, performed daily,
demonstrated the presence of renal tubular cells and
renal tubular cell casts. Surprisingly, it also showed
the presence of trophozoites of the protozoan Balantidium coli, which were identified on the basis of
its characteristic morphology and rapid movements
across the slide, and transient leukocyturia. The patient was asymptomatic, his medical history was negative for gastrointestinal disease, and no Balantidium
coli was found in the feces. In spite of this, due to the
previous chemotherapy, the patient was treated with
oral metrodinazole. Only one other case with Balantidium coli in the urine sediment has been described
so far and this paper stresses the importance of the
examination of the urinary sediment.
Key words: Balantidium coli, Protozoan, Trichomonas

vaginalis, Urinary balantidiasis, Urinary sediment

Balantidium coli is the largest protozoan that can infect humans and non-human primates. In swine, the usual host,
the infection remains silent. Human infection is rather un732

Department of Internal Medicine, Universit degli Studi

di Milano, IRCCS Fondazione Ca Granda-Ospedale
Maggiore Policlinico, Milan - Italy
Department of Nephrology (Research Laboratory on
Urine), IRCCS Fondazione Ca Granda-Ospedale
Maggiore Policlinico, Milan - Italy
Department of Microbiology, IRCCS Fondazione Ca
Granda-Ospedale Maggiore Policlinico, Milan - Italy

common and occurs most frequently in tropical and subtropical areas through the indirect fecal-oral route (1). Most
cases are asymptomatic or associated with gastrointestinal
symptoms. However, especially in immunocompromised
subjects, the disease may also involve the liver, the lungs or
the genitourinary system.
In this case report we describe an immunocompromised
patient hospitalized for acute kidney injury whose urine sediment, examined by an expert with conventional technology,
showed the presence of Balantidium coli.

Case report
On August 12, 2009 a 56-year-old Caucasian man was
admitted to our renal unit for acute renal failure. This had
been diagnosed the day before in the hematologic clinic,
where the patient was receiving follow-up care for a nonHodgkins lymphoma diagnosed in 2003. In that year, the
patient had been treated with six cycles of vincristine and
cyclophosphamide (CVP regimen) for four months, then
with six cycles of cisplatin, epirubicin and cyclophosphamide (PEC regimen) and finally with two cycles of high
dose cytarabine, cisplatin and dexamethasone (DHAP
regimen) for relapses. In 2006, the patient underwent a
peripheral stem cell transplantation (PBSC), after which a
complete clinical remission was achieved.
In January 2008, a diffuse recurrence of disease was diagnosed. Thus, the patient was treated with prednisolone,
cyclophosphamide, vincristine, doxorubicin and rituximab
(R-CHOP regimen). In November 2008, due to a further
progression of the disease, the patient was given the first
course of a hyper-CVAD regimen (cyclophosphamide, vin-

2010 Societ Italiana di Nefrologia - ISSN 1121-8428

JNEPHROL 2010 ; 23 ( 06 ) : 732 - 737

Fig. 1 - Left. Two trophozoites of

Balantidium coli. Phase contrast
microscopy makes it possible to
clearly identify the macronucleus
(arrow), the micronucleus (arrowhead) and the cilia which cover the
protozoan body (original magnification 400x). Right. Drawing representation of a trophozoite (top) and its
typical movement through the slide
(bottom) (modified from reference
19, reproduced with permission).

cristine, doxorubicin, dexamethasone, cytarabine, methotrexate), which in August 2009 was followed by a second
course based on methotrexate, leucovorin and cytarabine.
This was complicated by sepsis sustained by Escherichia
coli, for which the patient was given meropenem 1 g three
times/day intravenously for several days. At discharge, the
patient was prescribed oral ciprofloxacin 500 mg twice/day
and prophylactic oral fluconazole, 200 mg/day. At that time
his serum creatinine was 1.1 mg/dL and urinalysis normal.
However, seven days later, when tested at the clinic, serum
creatinine was found to be 4.0 mg/dL. The patient was accordingly hospitalized in our unit.
The clinical history revealed that two days before the patient was admitted, he had taken one tablet of nimesulide
(100 mg) for arthralgia, and that he had also had a transient
episode of very marked sweating, without any weight loss,
however. At physical examination, the patient was afebrile,
normotensive, without symptoms or signs of dehydration.
Serum creatinine was 3.9 mg/dL, WBC count was 8100/L
and hemoglobin level 111 g/L. CRP was 2.1 mg/dL (normal
value <0.5). Serum electrolytes, C3 and C4 serum levels,
ANCA test, liver function tests, acid-base balance were all
Urinalysis, by dipstick, showed pH 5.0, specific gravity 1.008
and negative albumin, hemoglobin, leukocyte esterase and
nitrites. Urine proteins, measured by benzetonium chloride,
were absent. The urinary sediment, examined by phase
contrast microscopy, showed 1 renal tubular epithelial cell
(RTEC) every 2 to 3 high power fields (HPF)(400x) asso-

ciated with a ++++ cylindruria (>1 cast/low power field

at 160x) due to hyaline, hyaline-granular and RTEC casts,
without any other particles.
All these findings were indicative of a condition of acute kidney injury with tubular damage (2), which might have been
caused by nimesulide, cyprofloxacin, and/or transient dehydration due to heavy sweating.
Therefore, ciprofloxacin was withdrawn and the patient was
put on oral hydration with 3 L of water/day.
During the following 8 days, serum creatinine progressively
decreased to the basal value of 0.9 mg/dL, while repeated
urine sediment examinations showed a progressive reduction of the number of RTECs and RTEC casts up to their
complete disappearance.
However, on August 17, some oval and ciliated organisms
which moved very rapidly across the slide with frequent circular turnings were also found in the urinary sediment. They
were 21 to 48 m in length and 12 to 24 m in width and
contained two nuclei (one elongated and the other smaller
and round) and many cytoplasmic vacuoles (Fig. 1). The cilia
were all of the same length and showed constant, fast and
synchronized motion. These features were consistent with
the identification of Balantidium coli trophozoites.
On the following two days, the urine sediment showed mild
leukocyturia (1-2 WBC/HPF) without bacteriuria, which was
confirmed by a 1+ positivity for leukocyte esterase by dipstick. A very careful examination of many different slides
from a large number of different samples did not reveal any
presence of Balantidium coli.

Maino et al: Balantidium coli in urine

After these findings, a search of Balantidium coli in the

feces was performed, which turned out to be negative in
6 out of 6 samples. On questioning, the patient denied
direct contact with swine, attending overcrowded institutional environments, or visits to tropical or subtropical areas. He also denied diarrhea, other gastrointestinal
symptoms, previous urinary tract infections or urethral
discharge. However, in consideration of his prolonged
chemotherapy, the patient was treated with oral metronidazole, 250 mg three times daily for one week.
The patient was discharged in good general conditions
with the diagnosis of multifactorial and reversible acute
renal injury and urinary balantidiasis in a patient with nonHodgkins lymphoma.

Balantidium coli, originally described by Malmsten in 1857
(3), is a large ciliated protozoan with worldwide distribution.
It has a trophozoite phase (i.e., an activated feeding stage in
the life of a protozoan parasite) and a cyst phase.
The trophozoites are ovoid in shape, measure 30 to 150
m in length and 25 to 120 m in width, contain two nuclei (one sausage-shaped macronucleus and one rounded micronucleus) and several contractile vacuoles (1).
The oral apparatus (cytostome) is located at the tapering
anterior end and the anus (cytopyge) at the rounded posterior end (Fig. 1). The organism is completely covered
by short and mobile cilia.
The cysts are the transmissive stage of the organism. They
are ovoid or spherical and measure 45 to 65 m in diameter
(1). The process of encystment begins in the colon and rectum of the host, and cysts are generally found in feces.
The natural habitat of Balantidium coli is the large intestine
of both pigs and humans, even though it may also be found
in wild rats, chimpanzees, orangutans and, infrequently,
dogs or cats (1). Human infection usually occurs through
contact with swine fecal matter. Ingestion of cysts by contaminated food is followed by excystation and releases
of trophozoites that invade the colonic mucosa with consequent inflammation, ulcers and abscesses which may
reach the muscular layer (1).
Direct or indirect frequent contacts with swine and scarce
hygienic conditions in tropical and subtropical areas favor
human balantidiasis, even though sporadic cases may
occur in temperate or even cold climates. Other favoring factors are immunosuppression, as found in patients
with HIV/AIDS (4, 5) or with hematological malignancies
(6, 7), and overcrowded conditions as observed in mental
institutions (8, 9). In this last respect, however, Balan734

tidium coli was found in the feces of only one subject out
of 238 residents of four Italian mental centers (10).
The worldwide prevalence of Balantidium coli infection
accounts for 0.02 to 1% (1) with peaks up to 28% among
pig farmers in New Guinea (11).
Three clinical presentations due to Balantidium coli are possible: asymptomatic carrier; chronic infection, with diarrhea alternating with constipation and unspecific abdominal symptoms; acute fulminating and life-threatening bloody diarrhea
due to intestinal ulcers and/or perforation (1). Extraintestinal
disease is also possible, with appendix (12), peritoneal (13),
pulmonary (14) and genital involvement (15, 16).
Urinary balantidiasis has very rarely been reported. In 1998,
Maleky described a 45-year-old woman from Iran who presented with burning abdominal pain in whom cystoscopy
showed diffuse patchy cystitis associated with Balantidium
coli trophozoites in bladder mucosa (17). More recently,
Umesh reported a 29-year-old Indian woman with symptomatic cystitis due to Balantidium coli whose trophozoites
were repeatedly found in the urine sediment (18). Symptoms
subsided with specific treatment of tetracycline and metronidazole for seven days. Thus, our patient is only the second
person reported in the literature to have been found with
Balantidium coli in the urinary sediment.
In our patient, who can be considered an asymptomatic
carrier, a few aspects deserve a comment. The first is that
the presence of Balantidium coli was followed by a transient
leukocyturia, which was absent in the previous days. This
fact demonstrates that Balantidium coli caused an inflammatory reaction in the urinary system. The second aspect is
the quick disappearance of Balantidium coli from the urine
and the negative results of the search for Balantidium coli in
several fecal samples. This fact, however, is well known and
typical of Balantidium coli (1). Another interesting issue is
how the protozoan reached the urine in the absence of diarrhea and/or urethritis, which are well known factors favoring
the spreading of Balantidium coli to the urinary system (15,
16). Thus, it might be postulated that the intestinal tract infection could have invaded the intestinal mucosa, entered
the blood stream and involved the urinary system (18). A
final aspect is that the source of Balantidium coli infection
remains unclear in this patient, even though the heavy and
prolonged chemotherapy he had received for his lymphoma
was a strong favoring factor.
In urine sediments, another protozoan can be found,
namely Trichomonas vaginalis. It has a round to pyriform
shape, 7 to 23 m in length and 5 to 15 m in width. Its
distinguishing morphological feature is the presence of
four anterior flagella and one flagellum bent backwards,
which is linked to the body by an undulating membrane

JNEPHROL 2010 ; 23 ( 06 ) : 732 - 737

Fig. 2 - Left. Bottom: a trophozoite

of Trichomonas vaginalis in the urine
sediment with the typical pyriform
shape, the anterior flagella (arrowhead) and the posterior flagellum (arrow); top: a dead trophozoite whose
flagella are no longer evident (phase
contrast microscopy, original magnification 400x). Right. Drawing representation of a Trichomonas vaginalis trophozoite (top) and its typical
movement through the slide (bottom)
(modified from reference 19, reproduced with permission).

(Fig. 2). When alive, Trichomonas vaginalis also shows

quick movements through the slide, which are due to the
motility of the flagella. The movements differ remarkably,
however, from those of Balantidium coli, since Trichomonas vaginalis whirls and turns in all directions, seem-

ing to vibrate (Fig. 2) (19). On the contrary, when dead,

Trichomonas vaginalis can easily be misidentified since it
is similar to polymorphonuclear leukocytes. Table I shows
the morphological differences between Balantidium coli
and Trichomonas vaginalis as seen in urine sediments.



Balantidium coli

Trichomonas vaginalis

Oval with one pole more rounded than the other

Round to pyriform

Size (m)

30-150 (length)
25-120 (width)

7-23 (length)
5-15 (width)


One sausage-shaped macronucleus

One round micronucleus

One ovoid


Transparent containing many contractile vacuoles

Finely granular


Short cilia covering the whole protozoan body with

fast and synchronized motion

Four anterior flagella and a posterior

flagellum bent backward

Very rapid with frequent circular turnings

Whirls and turns in all directions seeming to vibrate


Movement through
the slide


Maino et al: Balantidium coli in urine

In urine sediments, Trichomonas vaginalis is not as rare

as Balantidium coli (in our laboratory, 2 positive samples
out of 2,744 in the last 12 months), and it usually indicates contamination from genital secretions. Trichomonas
vaginalis is usually responsible for sub-acute or chronic
vaginitis, which may be complicated by urethritis, cystitis, cervicitis and salpingitis (20). In such cases, the urine
sediment contains not only Trichomonas vaginalis but also
polymorphonuclear leukocytes and bacteria and, quite often, also Candida albicans.

We would like to conclude this paper by stressing that Balantidium coli infection would have not been diagnosed in
our patient if the urinary sediment had not been examined
daily and carefully by expert personnel. This fact confirms
previous reports (21-23) which demonstrated that the examination of urinary sediment, in skilful hands, has an added
value compared to the examination carried out in centralized clinical laboratories.
In order to improve the impact of urine sediment examination on clinical practice, we think that: 1. nephrologists
should know more about the information on the diseases


Schuster FL, Ramirez-Avila L. Current world status of Balantidium coli. Clin Microbiol Rev. 2008;21:626-638.
2. Perazella MA, Coca SG, Kanbay M, Brewster UC, Parikh CR.
Diagnostic value of urine microscopy for differential diagnosis
of acute kidney injury in hospitalized patients. Clin J Am Soc
Nephrol. 2008;3:1615-1619.
3. Malmsten PH. Infusorien als Intestinal-Thiere bei Menschen (Human intestinal parasites). Arch Pathol Anat
Physiol Klin Med. 1857;12:302-309.
4. Clyti E, Aznar C, Couppie P, Guedj M, Carme B, Pradinaud R.
A case of coinfection by Balantidium coli and HIV in French
Guiana. Bull Soc Pathol Exot. 1998;91:309-311.


affecting the urinary tract that can be obtained through this

inexpensive, bedside diagnostic tool; 2. it should become
a procedure that is commonly performed by nephrologists
themselves, whose capability to identify the most important particles of the urine sediment seems to be insufficient
nowadays (24); 3. each renal unit should have at least one
nephrologist particularly skilled in urinary microscopy, who
can correlate the microscopic and physicochemical findings
of the urine with the results of other laboratory tests and the
clinical features of the patients.
Financial support: No financial support.
Conflict of interest statement: None declared.

Address for correspondence:

Giovanni Battista Fogazzi
Department of Nephrology
Research Laboratory on Urine
IRCCS Fondazione Ca Granda
Ospedale Maggiore Policlinico
Via Commenda, 15
20122 Milan, Italy





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Received: October 26, 2009

Revised: December 09, 2009
Accepted: January 21, 2010