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Chronic Diarrhea from Capillaria philippinensis in Mindoro
81VOL. 46 NO. 3 2012 ACTA MEDICA PHILIPPINAVol. 43 N0. 4 2009 ACTA MEDICA PHIlIPPINA 13
Heart Failure and Short Stature in a 43 year-old male
transferred to the intensive care unit (ICU) for ventilatory
supportandclosermonitoring.onbedsidecardiacultrasound,
there was a finding of eccentric left ventricular hypertrophy,
global hypokinesia with depressed overall systolic function
withconcomitantspontaneousechocontrastonleftventricular
(lV) cavity suggestive of rheologic stasis, the ejection fraction
was 25%, with moderate mitral regurgitation, moderate
aortic regurgitation with aortic sclerosis, severe tricuspid
regurgitation with mild pulmonary hypertension, pulmonary
regurgitation, and minimal pericardial effusion or pericardial
fat pad. Cardiac enzymes were not consistent with an acute
coronary event (Table 3), however, intravenous (IV) heparin
(overlapping with oral warfarin) was still given to cover for
the presence of a possible lV thrombus as demonstrated
by rheologic stasis on cardiac ultrasound. Medications
were shifted to IV diuretics and inotropes; oral digoxin was
started. IV antibiotics were given for possible pulmonary
infection. The patient later on showed improvement, and was
eventually weaned off from ventilatory support, extubated,
Table 1. Initial laboratory Results
WBC
RBC
HGB
HCT
MCV
MCH
MCHC
RDW
PlT
RETIC
SEG
lYMPH
MoNo
Eo
BASo
BlAST
CBC
Reference
Value
5-10
4-6
120-150
0.38-0.48
80-100 Fl
27-31 PG
320-360 G/l
11.5-15.5%
200-400
0.005-0.015
50-70%
20-44%
2-9%
0-4%
0-2%
0%
Result
4.5
90
0.27
Inc
48
50
2
0
0
0
RBS
HGBA1C
BUN
CREA
AlB
TAG
HDl
lDl
ToTAl CHol
AST
AlT
Alk po4
NA
K
Cl
CA++
P
MG++
Reference
Value
3.9-6.1
4.27-6.07
2.6-6.4
53-115
34-50
0.34-1.7
0.91-1.56
1.1-3.8
4.2-5.2
15-37
30-65
140-148
3.6-5.2
100-108
2.12-2.52
0.74-1
Result
6.3
6.4
5.0
123
32
0.82
0.67
4.21
5.25
95
91
184
136.9
3.35
86
2.37
2.27
0.83
Blood chem.
Color
Transp
Sp Gravity
pH
Sugar
Protein
RBC
WBC
Cast
Epith cell
Bacteria
Mucus th
Crystals
Am urates
straw
Clear
1.010
8.0
NEG
NEG
0-1
0-2
Rare
occ’l
Rare
Rare
Urinalysis
pH
pCo2
po2
HCo3
o2 sat
Fio2
Temp
7.408
49.1
70
31.3
93.6
21%
36.9
ABG
PBS
Slight poikilocytosis,
acanthocytes, ovalocytes,
slight toxic granulation,
slight anisocytosis
Table 2. Thyroid Function Tests
Free T4
TSH
(0.8-2.0)
(0.4-6.0)
0.02 ng/dl
24.75 Uiu/ml
Reference Value Result
Figure 1. Electrocardiogram upon admission
Table 3. Cardiac Enzymes
Qualitative
Troponin I
CK-MB
CK-ToTAl
0-6.0
21-232
PoSITIVE
1.14
543
Reference Range (mmoL) Result
Figure 2. Chest radiograph on admission
_______________
Corresponding author: Mary Ondinee U. Manalo, MD
Department of Medicine
Philippine General Hospital
University of the Philippines Manila
Taft Avenue, Ermita, Manila 1000 Philippines
Telephone: +632 8062209 / 0923 6503548
Email: marymanalo_md@yahoo.com
A Case of Chronic Diarrhea Secondary to Capillaria philippinensis in
Occidental Mindoro: Possibly a Newly-Described Endemic Area?
Mary Ondinee U. Manalo,1 Virgilio P. Bañez2 and Vicente Y. Belizario, Jr.3,4
1Department of Medicine, College of Medicine and Philippine General Hospital, University of the Philippines Manila
2Section of Gastroenterology, Department of Medicine, College of Medicine and Philippine General Hospital, University of the Philippines Manila
3National Institutes of Health, University of the Philippines Manila
4Department of Parasitology, College of Public Health, University of the Philippines Manila
Introduction
Intestinal capillariasis or capillariasis philippinensis is
caused by a small nematode known as Capillaria
philippinensis. Symptoms of this illness are diarrhea,
borborygmi, and abdominal pain. This helminthic infection
was virtually unknown until 1963 when Chitwood reported
the first case, a schoolteacher from Bacarra, Ilocos Norte. He
had a history of intractable diarrhea for 3 weeks with ascites,
emaciation and cachexia and later died at the Philippine
General Hospital in Manila.1,2
In the 1960s, a capillariasis outbreak occurred in
Tagudin, Ilocos Sur where almost a hundred died.3 Another
epidemic was recorded in Southern Leyte in the Philippines
in the early 1980s.4 In the recent past, this parasite was also
isolated in Compostela Valley Province2 and Zamboanga del
Norte in Western Mindanao.5
We present a case of chronic diarrhea secondary to
multiple enteric pathogens, including Capillaria philippinensis
in Occidental Mindoro, a possible newly-described endemic
area.
Case
A 41-year-old male from the town of Alacaak, Sta. Cruz,
Occidental Mindoro presented with a one-year history of
colicky abdominal pain and watery diarrhea. Multiple
consults were done in their region that revealed
“unremarkable fecalyses”. He was given various antibiotics
but this did not resolve his symptoms.
Six months prior to admission, four men in their
barangay died from chronic diarrhea and this prompted the
patient to seek consult in Manila. He was admitted in a
private hospital for work-up where fecalysis again was
“unremarkable”, abdominal CT that revealed no masses,
and colonoscopy with biopsy that revealed mild nonspecific
colitis. During this time, the patient had lost more than a
third of his weight and developed bipedal edema. Patient
was repeatedly readmitted but no definite diagnosis was
established. He was never febrile.
The patient had a history of pulmonary tuberculosis
treated for only a week. He was fond of eating dogs and
kilawin. He knew the four people who died in their locality.
He admitted to having been in a drinking binge with at least
one of them and ate kilawin during their binges. He worked
as a farmer, as a fisherman, and as a tricycle driver. He
would catch fish in Pagbahan River, but would sometimes
buy from the local market. No other family member
presented with diarrhea. He had no history of travel.
The patient presented at the Emergency Room of the
Philippine General Hospital severely emaciated, unable to
ambulate and with palpatory BP (Figure 1). He weighed 42
kilograms (BMI=16), with bronchovesicular breath sounds,
normal cardiac rate and regular rhythm, scaphoid abdomen
which was normoactive, grade 2 bipedal non-pitting edema,
and unremarkable digital rectal exam. Neurologic findings
were normal. He was hydrated and started on inotropes.
Initial investigations revealed the following: severe
hypoalbuminemia (2g/L) with no proteinuria, hemoglobin
142g/L, wbc 7.4 x 109/L (neut 0.64 lymph 0.32 eos 0.013), and
low electrolytes (sodium, potassium, calcium, magnesium,
and phosphorus). He had normal creatinine, bilirubins, and
liver enzymes. His ECG had low voltage complexes. His
initial stool examination showed abundant white blood
cells, without any RBC, fat globules, ova, or parasites. Fecal
CASE REPORT
Chronic Diarrhea from Capillaria philippinensis in Mindoro
82 VOL. 46 NO. 3 2012ACTA MEDICA PHILIPPINA Vol. 43 N0. 4 200912 ACTA MEDICA PHIlIPPINA
Heart Failure and Short Stature in a 43 year-old male
Katerina T. leyritana1
, Ma. Czarlota M. Acelajado-Valdenor1
, Amado o. Tandoc III2
and Agnes D. Mejia1
1
Department of Medicine, College of Medicine and Philippine General Hospital, University of the Philippines Manila
2
Department of Pathology, College of Medicine, University of the Philippines Manila
CASE REPORT
Corresponding author: Ma. Czarlota Acelajado-Valdenor, M.D.
Department of Medicine
Philippine General Hospital
Taft Avenue, Manila, 1000 Philippines
Telephone: +632 554-8488
Email: czarlota@yahoo.com
Presentation of the case
This is a case of a 43-year-old male presenting with short
stature and heart failure. The patient was admitted at the
medicine ward of the Philippine General Hospital (PGH)
for dyspnea. This paper will investigate several issues:
differentiating congenital from acquired hypothyroidism,
the relationship between hypothyroidism and the
cardiomyopathies, and the therapeutic options in patients
with cardiomyopathy secondary to hypothyroidism.
The patient had been born full term to a then 31-year-
old Gravida 4 Para 3 (G4P3), the 4th
of 9 siblings, with an
apparently unremarkable delivery at home facilitated by
a traditional birth attendant. He was noted to be normal
at birth. The patient was allegedly at par with age both
physically and mentally until eight years old when he was
said to have stopped growing in height. He was brought to
a private doctor, whose diagnosis was undisclosed, and he
was given medications to increase height, which the patient
took for only one month with no improvement. Through the
years, the patient was apparently well, although still of short
stature, with thick lips, coarse facial features and dry skin.
He was notably slow in ambulation. He was said to have
bronchial asthma at age 15 years, and since then he had been
taking salbutamol tablets occasionally for bouts of dyspnea
occurring one to two times annually.
The patient’s symptoms started in 2001 when he was
reported to have sudden loss of consciousness. During this
time, the patient did not have any symptoms of heart failure;
no prior seizures, cyanotic episodes, chest pain, headache, or
blurring of vision. He regained consciousness shortly after and
was brought to a private physician, whose assessment was a
“heart problem”. He was prescribed unrecalled medications
taken for a few months and eventually discontinued when
the syncopal episode did not recur.
In the next four years, the patient would develop
intermittent, progressive exertional dyspnea and bipedal
edema. later on this would be accompanied by generalized
body weakness, anorexia, and constipation, severe enough to
require regular laxative use. There was also a report of two
more syncopal episodes. He was brought to another doctor
in a private hospital where the assessment was still a “heart
problem”. The patient was again prescribed unrecalled
medications and again was lost to follow-up. This time,
however, symptoms were persistent. He later consulted at
another local hospital, where he was admitted and managed
as a case of anemia and bronchial asthma. He was discharged
slightly improved after four days, only to have recurrent heart
failure symptoms, prompting admission at PGH.
Upon admission the patient was in mild respiratory
distress, with stable vital signs and no note of fever. Pertinent
physical exam findings included short stature, thick lips, non-
pitting periorbital edema, dry skin, a displaced apical impulse,
crackles on both lung fields, and bilateral non-pitting bipedal
edema. There was also a 3 cm x 3 cm reducible umbilical
hernia. However, there was no pallor, no neck vein distention,
no apparent congenital malformations, no cardiac murmurs
and no clubbing. There was also no note of an anterior neck
mass.
laboratoryworkupshowedcardiomegalywithpulmonary
congestion,thoracicdextroscoliosis,andatheromatousaortaby
chest radiograph, and left ventricular hypertrophy by 12-lead
electrocardiogram (12-l ECG) (Figures 1 and 2), normocytic
normochromic anemia (Hgb 90 mg/dl), dyslipidemia, and
pre-renal azotemia (serum creatinine 123 mmol). Electrolytes
on admission showed slight hyponatremia, hypokalemia,
and hypochloremia (serum Na 136, K 3.35, Cl 86). Blood gases
revealed partially compensated metabolic alkalosis with mild
hypoxemia. The patient was noted to be hypothyroid based
on elevated serum thyroid-stimulating hormone (TSH) and
markedly decreased serum free thyroxine (FT4). The exact
values are shown in Tables 1 and 2.
Upon admission to the wards, the patient was managed
as having congestive heart failure from cardiomyopathy
secondary to acquired hypothyroidism. oral loop diuretics,
angiotensin-converting enzyme (ACE) inhibitors, beta-
blockers, statins, and levothyroxine were started. Electrolyte
correction was instituted. The sections of Endocrinology
and Cardiovascular Diseases were co-managing the patient
together with the General Medicine service.
He soon developed respiratory failure, upon which the
considerations were acute pulmonary congestion, nosocomial
pneumonia, to rule out an acute coronary event. He was later
occult blood was likewise negative. Investigations for
pulmonary tuberculosis including a chest film and sputum
AFB were normal. No enteric pathogen was isolated on
initial stool culture. Stool was sent to the College of Public
Health for FECT which revealed no parasites. A 2D-echo
was requested to rule out a cardiogenic cause for the shock
and it revealed a small pericardial effusion with an ejection
fraction of 33%.
Figure 1. Appearance of the patient prior to treatment
(BMI=16 kg/m2).
Since no enteric pathogen was initially isolated, the
investigator initially pursued work-up for non-infectious
causes like malabsorption syndromes, irritable bowel
disease, malignancy, adrenal insufficiency,
hyperthyroidism, and carcinoid. Infectious causes were
likewise pursued. Cortisol (560 pmol/L) and thyroid
function tests were both normal. Irritable bowel disease and
malignancy were ruled out because of the CT scan and the
colonoscopy findings. Another stool culture was done and
this revealed growth of Candida species. Salmonella IgG/IgM
were non-reactive. HIV screening was negative. Stool AFB
was +1 on day 1 and day 2. However, the investigator was
not entirely convinced that this was just TB and stool was
sent almost every day for fecalysis.
The patient was on inotropes and colloids during the
first week of his admission. He was placed on nothing per
orem, except medications, to allow time for the patient’s
intestinal villi to regenerate. Gastroenterology consult was
sought and the patient was treated as if he had short gut
syndrome. He was started on ranitidine, loperamide, and
racecadotril. Fluconazole and Category I TB treatment were
started as well. He was placed on total parenteral nutrition.
By the end of the second week, patient was off inotropes
and was started on clear liquids. When this was tolerated,
he was started on elemental feeding.
However, diarrhea persisted. By the third week, serial
fecalyses revealed the presence of the following: Entamoeba
histolytica cysts, Strongyloides stercoralis adult and
rhabditiform larvae. First line treatment for strongyloidiasis
is Ivermectin but this was not available in the Philippines.
Second line drug is albendazole 400 mg bid x 5 days every 2
weeks x 2 cycles and this was started on the patient the
same day. Since the patient had been treated multiple times
for amoebiasis, diloxanide furoate, a luminal agent, was
added on top of metronidazole.
The next stool sample had suspected Capillaria
philippinensis ova, which were atypical because they did not
possess bipolar plugs. Another stool sample was sent the
following day and the diagnosis of capillariasis was
established when it revealed typical Capillaria ova with
bipolar plugs (Figure 2). The patient was then treated with
the following drugs: albendazole 400 mg bid x 10 days then
repeated after 2 weeks (this covered for both C. philippinensis
and S. stercoralis); metronidazole 500 mg tabs q6 x 14 days;
diloxanide furoate 500 mg tab tid x 14 days; fluconazole 200
mg cap x 10 days; and quadruple anti-Koch’s. By this time,
the chronic diarrhea of the patient was attributed to: 1.) TB
colitis, 2.) C. philippinensis, 3.) S. stercoralis, 4.) E. histolytica,
and 5.) C. albicans.
Figure 2. C. philippinensis ova recovered from the stool of the
patient.
Three days after being given those drugs, diarrhea
resolved. A repeat 2D-Echo showed an improved ejection
fraction of 72%, consistent with nutritional cardiomyopathy.
After another week, the patient was discharged wheelchair-
borne. He was educated on how he acquired his illness.
Avoidance of eating raw fish and walking barefooted was
emphasized. A month after, the patient followed up
weighing 49 kg (Figure 3). He was already ambulant and
had good appetite. Albumin improved from 2 g/L to 24 g/L
after just one month. Repeat FECT revealed no organisms.
By the time he completed his 6 months of anti-Koch’s, he
was already back in Occidental Mindoro where he now
drives his tricycle for a living.
Chronic Diarrhea from Capillaria philippinensis in Mindoro
83VOL. 46 NO. 3 2012 ACTA MEDICA PHILIPPINAVol. 43 N0. 4 2009 ACTA MEDICA PHIlIPPINA 13
Heart Failure and Short Stature in a 43 year-old male
transferred to the intensive care unit (ICU) for ventilatory
supportandclosermonitoring.onbedsidecardiacultrasound,
there was a finding of eccentric left ventricular hypertrophy,
global hypokinesia with depressed overall systolic function
withconcomitantspontaneousechocontrastonleftventricular
(lV) cavity suggestive of rheologic stasis, the ejection fraction
was 25%, with moderate mitral regurgitation, moderate
aortic regurgitation with aortic sclerosis, severe tricuspid
regurgitation with mild pulmonary hypertension, pulmonary
regurgitation, and minimal pericardial effusion or pericardial
fat pad. Cardiac enzymes were not consistent with an acute
coronary event (Table 3), however, intravenous (IV) heparin
(overlapping with oral warfarin) was still given to cover for
the presence of a possible lV thrombus as demonstrated
by rheologic stasis on cardiac ultrasound. Medications
were shifted to IV diuretics and inotropes; oral digoxin was
started. IV antibiotics were given for possible pulmonary
infection. The patient later on showed improvement, and was
eventually weaned off from ventilatory support, extubated,
Table 1. Initial laboratory Results
WBC
RBC
HGB
HCT
MCV
MCH
MCHC
RDW
PlT
RETIC
SEG
lYMPH
MoNo
Eo
BASo
BlAST
CBC
Reference
Value
5-10
4-6
120-150
0.38-0.48
80-100 Fl
27-31 PG
320-360 G/l
11.5-15.5%
200-400
0.005-0.015
50-70%
20-44%
2-9%
0-4%
0-2%
0%
Result
4.5
90
0.27
Inc
48
50
2
0
0
0
RBS
HGBA1C
BUN
CREA
AlB
TAG
HDl
lDl
ToTAl CHol
AST
AlT
Alk po4
NA
K
Cl
CA++
P
MG++
Reference
Value
3.9-6.1
4.27-6.07
2.6-6.4
53-115
34-50
0.34-1.7
0.91-1.56
1.1-3.8
4.2-5.2
15-37
30-65
140-148
3.6-5.2
100-108
2.12-2.52
0.74-1
Result
6.3
6.4
5.0
123
32
0.82
0.67
4.21
5.25
95
91
184
136.9
3.35
86
2.37
2.27
0.83
Blood chem.
Color
Transp
Sp Gravity
pH
Sugar
Protein
RBC
WBC
Cast
Epith cell
Bacteria
Mucus th
Crystals
Am urates
straw
Clear
1.010
8.0
NEG
NEG
0-1
0-2
Rare
occ’l
Rare
Rare
Urinalysis
pH
pCo2
po2
HCo3
o2 sat
Fio2
Temp
7.408
49.1
70
31.3
93.6
21%
36.9
ABG
PBS
Slight poikilocytosis,
acanthocytes, ovalocytes,
slight toxic granulation,
slight anisocytosis
Table 2. Thyroid Function Tests
Free T4
TSH
(0.8-2.0)
(0.4-6.0)
0.02 ng/dl
24.75 Uiu/ml
Reference Value Result
Figure 1. Electrocardiogram upon admission
Table 3. Cardiac Enzymes
Qualitative
Troponin I
CK-MB
CK-ToTAl
0-6.0
21-232
PoSITIVE
1.14
543
Reference Range (mmoL) Result
Figure 2. Chest radiograph on admission
Figure 3. The patient after treatment (BMI=20 kg/m2).
Discussion
Capillariasis is a parasitic disease caused by infection
with any of the four Capillaria species found to infect
humans: Capillaria hepatica, C. aerophila, C. plica, and C.
philippinensis.3 Capillaria philippinensis inhabits the small
bowel of humans, causing mostly diarrhea and
malabsorption. The life cycle is incompletely understood,
although freshwater fish contain larvae infectious for
humans and birds. The latter is an important reservoir host,
especially migratory birds that could drop their feces in any
body of water. Laboratory examinations document the
typical findings of protein-losing enteropathy,
malabsorption, and electrolyte loss. The diagnosis is
established by detecting characteristic ova or larvae in the
stool. In untreated patients, mortality rate is 33%, but
specific anti-helminthic therapy is effective and life-saving.
Infection is prevented by eating only properly cooked
freshwater fish.6
C. philippinensis was first reported in 1963 in Bacarra,
Ilocos Norte Province and has been endemic in that area
ever since, particularly in Pudoc Lake where it was isolated.1
Since then, additional endemic foci of C. philippinensis have
been identified in Southern Leyte,3 in Compostela Valley, in
Southern Mindanao,2 and in Zamboanga del Norte, Western
Mindanao.5
To date, this is the first reported case of intestinal
capillariasis from Occidental Mindoro, an island bounded
by the Mindoro Strait and the Mamburao reef (Figure 4).
There are 11 barangays in Sta. Cruz, and in Alacaak, where
the patient resides, there is a freshwater reservoir called the
Pagbahan River where he sometimes catches fish. People
here are fond of eating kilawin, which is raw fish soaked in
vinegar and seasoning.
The lacustrine goby or dulong (Gobiopterus lacustris)
and the Philippine anchovy or bolinaw (Encrasicholina
oligobranchus) are the two most common species eaten raw
in their locality because they are cheap. In fact, they are
sometimes called the “poorman’s fish”. However, when
there is a festivity, they would sometimes use chopped
and pounded milkfish (Chanos chanos) or tanigue
(Acanthocybium solandri) in their kilawin. Any of these species
of fishes could have been harboring the infective larvae and
could have been ingested by migratory birds as the
definitive host or by men as the accidental host.
Figure 4. The Municipality of Sta. Cruz, Occidental Mindoro
(Source: www.wikipilipinas.org, reproduced with
permission).
According to the patient, people living here have water-
sealed toilets, although he is aware of some families using
pit privies. He also attested that some people in their locality
resort to open and indiscriminate defecation. Children
sometimes defecate near the shoreline when they are
playing and swimming.
In this case, we believe that the patient may be an
“indigenous case” in that he acquired his infection from his
locality (rather than an “imported case”, where a patient got
the infection from an already established endemic area). He
had no history of travel, and there were already 4 deaths in
their area attributed to diarrhea secondary to an
undetermined cause. Since migratory birds are in part
responsible for dissemination, the bodies of water
surrounding Sta. Cruz may have been part of their usual
stops. The cycle of fish eating infected feces, then man eating
infected fish could have easily been perpetuated in this area
because eating raw fish is a common practice. Furthermore,
since open and indiscriminate defecation has been described
by the patient, fish eating not just infected bird feces, but
infected human feces as well, could have been part of the
cycle.
This case presented with diagnostic difficulties since the
patient presented with almost a year of “unremarkable”
Chronic Diarrhea from Capillaria philippinensis in Mindoro
84 VOL. 46 NO. 3 2012ACTA MEDICA PHILIPPINA Vol. 43 N0. 4 200912 ACTA MEDICA PHIlIPPINA
Heart Failure and Short Stature in a 43 year-old male
Katerina T. leyritana1
, Ma. Czarlota M. Acelajado-Valdenor1
, Amado o. Tandoc III2
and Agnes D. Mejia1
1
Department of Medicine, College of Medicine and Philippine General Hospital, University of the Philippines Manila
2
Department of Pathology, College of Medicine, University of the Philippines Manila
CASE REPORT
Corresponding author: Ma. Czarlota Acelajado-Valdenor, M.D.
Department of Medicine
Philippine General Hospital
Taft Avenue, Manila, 1000 Philippines
Telephone: +632 554-8488
Email: czarlota@yahoo.com
Presentation of the case
This is a case of a 43-year-old male presenting with short
stature and heart failure. The patient was admitted at the
medicine ward of the Philippine General Hospital (PGH)
for dyspnea. This paper will investigate several issues:
differentiating congenital from acquired hypothyroidism,
the relationship between hypothyroidism and the
cardiomyopathies, and the therapeutic options in patients
with cardiomyopathy secondary to hypothyroidism.
The patient had been born full term to a then 31-year-
old Gravida 4 Para 3 (G4P3), the 4th
of 9 siblings, with an
apparently unremarkable delivery at home facilitated by
a traditional birth attendant. He was noted to be normal
at birth. The patient was allegedly at par with age both
physically and mentally until eight years old when he was
said to have stopped growing in height. He was brought to
a private doctor, whose diagnosis was undisclosed, and he
was given medications to increase height, which the patient
took for only one month with no improvement. Through the
years, the patient was apparently well, although still of short
stature, with thick lips, coarse facial features and dry skin.
He was notably slow in ambulation. He was said to have
bronchial asthma at age 15 years, and since then he had been
taking salbutamol tablets occasionally for bouts of dyspnea
occurring one to two times annually.
The patient’s symptoms started in 2001 when he was
reported to have sudden loss of consciousness. During this
time, the patient did not have any symptoms of heart failure;
no prior seizures, cyanotic episodes, chest pain, headache, or
blurring of vision. He regained consciousness shortly after and
was brought to a private physician, whose assessment was a
“heart problem”. He was prescribed unrecalled medications
taken for a few months and eventually discontinued when
the syncopal episode did not recur.
In the next four years, the patient would develop
intermittent, progressive exertional dyspnea and bipedal
edema. later on this would be accompanied by generalized
body weakness, anorexia, and constipation, severe enough to
require regular laxative use. There was also a report of two
more syncopal episodes. He was brought to another doctor
in a private hospital where the assessment was still a “heart
problem”. The patient was again prescribed unrecalled
medications and again was lost to follow-up. This time,
however, symptoms were persistent. He later consulted at
another local hospital, where he was admitted and managed
as a case of anemia and bronchial asthma. He was discharged
slightly improved after four days, only to have recurrent heart
failure symptoms, prompting admission at PGH.
Upon admission the patient was in mild respiratory
distress, with stable vital signs and no note of fever. Pertinent
physical exam findings included short stature, thick lips, non-
pitting periorbital edema, dry skin, a displaced apical impulse,
crackles on both lung fields, and bilateral non-pitting bipedal
edema. There was also a 3 cm x 3 cm reducible umbilical
hernia. However, there was no pallor, no neck vein distention,
no apparent congenital malformations, no cardiac murmurs
and no clubbing. There was also no note of an anterior neck
mass.
laboratoryworkupshowedcardiomegalywithpulmonary
congestion,thoracicdextroscoliosis,andatheromatousaortaby
chest radiograph, and left ventricular hypertrophy by 12-lead
electrocardiogram (12-l ECG) (Figures 1 and 2), normocytic
normochromic anemia (Hgb 90 mg/dl), dyslipidemia, and
pre-renal azotemia (serum creatinine 123 mmol). Electrolytes
on admission showed slight hyponatremia, hypokalemia,
and hypochloremia (serum Na 136, K 3.35, Cl 86). Blood gases
revealed partially compensated metabolic alkalosis with mild
hypoxemia. The patient was noted to be hypothyroid based
on elevated serum thyroid-stimulating hormone (TSH) and
markedly decreased serum free thyroxine (FT4). The exact
values are shown in Tables 1 and 2.
Upon admission to the wards, the patient was managed
as having congestive heart failure from cardiomyopathy
secondary to acquired hypothyroidism. oral loop diuretics,
angiotensin-converting enzyme (ACE) inhibitors, beta-
blockers, statins, and levothyroxine were started. Electrolyte
correction was instituted. The sections of Endocrinology
and Cardiovascular Diseases were co-managing the patient
together with the General Medicine service.
He soon developed respiratory failure, upon which the
considerations were acute pulmonary congestion, nosocomial
pneumonia, to rule out an acute coronary event. He was later
laboratory results. Capillariasis could possibly be endemic
in this barangay for quite some time now, but was left
undiagnosed. In Compostela Valley, there have been 12
deaths before the diagnosis of capillariasis was established.
This was attributed to the lack of proficiency of the local
health staff in laboratory diagnosis and a general lack of
awareness of this potentially fatal parasitic infection.2 An
inexperienced observer may confuse the eggs with those of
Trichiuris trichiura, which are larger (50 to 54 by 22 to 23 m)
and barrel-shaped, with more prominent mucoid bipolar
plugs.3
According to a study by Belizario et al., 54.7% of
patients examined at Compostela Valley were infected with
≥1 organism, including C. philippinensis. Most of the patients
were co-infected with hookworms, Endolimax nana,
Entamoeba histolytica, Entamoeba coli, and Heterphyes sp.2 This
is called polyparasitism, and the study done in Mindanao
reflected the same problem in Thailand where it is a
common practice to eat koi pla (chopped raw fish mixed with
lemon juice, finely cut red onion and chili) and tab kaab
(pounded raw whole fish mixed with lemon juice, finely cut
red onion and chili). C. philippinensis has been identified in
25 provinces in Thailand and majority of infected patients
also harbored hookworms.7,8 In addition, cases of
polyparasitism with C. philippinensis have also been reported
in Taiwan,9 Lao Republic,10 Egypt,11-12 Iran,13 Southern
Brazil14 and Africa.15
In our patient, the chronic diarrhea could have easily
been caused by C. philippinensis, S. stercoralis, and E.
histolytica. All these organisms are related to poor
environmental sanitation, possibly stemming from
indiscriminate defecation. Our patient was unique because
the Capillaria eggs only surfaced after more than 10 serial
fecalyses done at our Institution. This is odd, since Capillaria
infections are usually prolific. Eggs, larvae, and adults
appear in great numbers in stool specimens.3 This is in
contrast to S. stercoralis wherein worm load is low. In these
cases, chances of finding the parasite is proportional to the
number of occasions in which the stool is examined, or if
available, stool should be analyzed using concentration
techniques. It is also important to note that occurrence of
autoinfection, or the ability of a parasite to multiply and
complete one’s life cycle inside humans, is recognized only
in Strongyloides stercoralis and to a lesser extent, in Capillaria
philippinensis infections.16 In these two infections, complete
eradication of the parasite is necessary for cure.
The patient also had TB colitis, which is permissive for
infection with C. philippinensis and S. stercoralis.16 Parasitic
overgrowth rendered him susceptible to Candida as well. In
these cases of polyparasitism, morbidity becomes additive
and mortality subsequently is higher. The key then to the
cure of our patient was clinching the correct diagnosis that
facilitated correct treatment.
Conclusion
In summary, we have presented a case of intestinal
capillariasis from Occidental Mindoro, left undiagnosed for
more than a year in different institutions. Although
capillariasis contributed to his disease, polyparasitism with
Strongyloides stercoralis and Entamoeba histolytica could
account for the patient’s overall condition. Presently, there is
still a need to identify the possible occurrence of intestinal
capillariasis in other unrecognized foci and to define its
geographic distribution here and abroad.
Recommendations
This case was reported to the Department of Health to
pursue this site as a potential area for epidemiologic
investigation. Accurate diagnosis will result in the
appropriate treatment and provide information and
evidence as basis for the control and prevention of this
potentially fatal disease in the community.
__________
References
1. Chitwood MB, Valesquez C, Salazar NG. Capillaria philippinensis sp. nov.
(Nematoda: Trichinellida), from the intestine of man in the Philippines. J
Parasitol. 1968; 54(2):368-71.
2. Belizario VY, de Leon WU, Esparar DG, Galang JM, Fantone J,
Verdadero C. Compostela Valley: a new endemic focus for Capillaria
philippinensis. Southeast Asian J Trop Med Public Health. 2000; 31(3):478-
81.
3. Cross JH. Intestinal capillariasis. Clin Microbiol Rev. 1992; 5(2):120-9.
4. Cross JH, Basaca-Sevilla V. Biomedical Surveys in the Philippines. 1984;
NAMRU-2 SP-47:1-117.
5. Belizario VY, G Totañes FI, de Leon WU, Migriño JR Jr, Macasaet LY.
Intestinal capillariasis, Western Mindanao, the Philippines. Emerg Infect
Dis. 2010; 16(4):736-8.
6. Mandell GL, Bennett JE, Dolin R. Mandell, Douglas, and Bennett’s
Principles and Practice of Infectious Diseases, 7th
ed. Philadelphia, PA:
Churchill Livingstone, Elsevier; 2010.
7. Saichua P, Nithikathkul C, Kaewpitoon N. Human intestinal
capillariasis in Thailand. World J Gastroenterol. 2008; 14(4):506-10
8. Benjanuwattar T, Morakote N, Somboon P, Sivasomboon B. Intestinal
capillariasis: indigenous cases from Chiang Mai and Phayao provinces,
Thailand. J Med Assoc Thai. 1990; 73(7):414–7.
9. Bair MJ, Hwang KP, Wang TE, et al. Clinical features of human
intestinal capillariasis in Taiwan. World J Gastroenterol. 2004;
10(16):2391-3.
10. Soukhathammavong P, Sayasone S, Harimanana AN, et al. Three cases
of intestinal capillariasis in Lao People’s Democratic Republic. Am J
Trop Med Hyg. 2008; 79(5):735-8.
11. Austin DN, Mikhail MG, Chiodini PL, Murray-Lyon IM. Intestinal
capillariasis acquired in Egypt. Eur J Gastroenterol Hepatol. 1999;
11(8):935–6.
12. El-Kadi MA, Dorrah AO, Shoukry NM. Patients with gastrointestinal
complains due to enteric parasites, with reference to Entamoeba
histolytica/dispar as detected by ELISA E. histolytica adhesion in stool. J
Egypt Soc Parasitol. 2006; 36(1):53-64.
13. Rokni MB. The present status of human helminthic diseases in Iran. Ann
Trop Med Parasitol. 2008; 102(4):283-95.
14. Toledo MJ, Paludetto AW, Moura Fde T, et al. Evaluation of
enteroparasite control activities in a Kaingang community of Southern
Brazil. Rev Saude Publica. 2009; 43(6):981-90.
15. Crompton DW, Tulley JJ. How much Ascariasis is there in Africa?
Parasitol Today. 1987; 3(4):123-7.
16. Farthing M, Fedail S, Savioli L, Bundy DAP, Krabshuis JH. WGO
Practice Guideline Management of Strongyloidiasis. 2004.

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Capillaria philippinensis in Occidental Mindoro, Philippines

  • 1. Chronic Diarrhea from Capillaria philippinensis in Mindoro 81VOL. 46 NO. 3 2012 ACTA MEDICA PHILIPPINAVol. 43 N0. 4 2009 ACTA MEDICA PHIlIPPINA 13 Heart Failure and Short Stature in a 43 year-old male transferred to the intensive care unit (ICU) for ventilatory supportandclosermonitoring.onbedsidecardiacultrasound, there was a finding of eccentric left ventricular hypertrophy, global hypokinesia with depressed overall systolic function withconcomitantspontaneousechocontrastonleftventricular (lV) cavity suggestive of rheologic stasis, the ejection fraction was 25%, with moderate mitral regurgitation, moderate aortic regurgitation with aortic sclerosis, severe tricuspid regurgitation with mild pulmonary hypertension, pulmonary regurgitation, and minimal pericardial effusion or pericardial fat pad. Cardiac enzymes were not consistent with an acute coronary event (Table 3), however, intravenous (IV) heparin (overlapping with oral warfarin) was still given to cover for the presence of a possible lV thrombus as demonstrated by rheologic stasis on cardiac ultrasound. Medications were shifted to IV diuretics and inotropes; oral digoxin was started. IV antibiotics were given for possible pulmonary infection. The patient later on showed improvement, and was eventually weaned off from ventilatory support, extubated, Table 1. Initial laboratory Results WBC RBC HGB HCT MCV MCH MCHC RDW PlT RETIC SEG lYMPH MoNo Eo BASo BlAST CBC Reference Value 5-10 4-6 120-150 0.38-0.48 80-100 Fl 27-31 PG 320-360 G/l 11.5-15.5% 200-400 0.005-0.015 50-70% 20-44% 2-9% 0-4% 0-2% 0% Result 4.5 90 0.27 Inc 48 50 2 0 0 0 RBS HGBA1C BUN CREA AlB TAG HDl lDl ToTAl CHol AST AlT Alk po4 NA K Cl CA++ P MG++ Reference Value 3.9-6.1 4.27-6.07 2.6-6.4 53-115 34-50 0.34-1.7 0.91-1.56 1.1-3.8 4.2-5.2 15-37 30-65 140-148 3.6-5.2 100-108 2.12-2.52 0.74-1 Result 6.3 6.4 5.0 123 32 0.82 0.67 4.21 5.25 95 91 184 136.9 3.35 86 2.37 2.27 0.83 Blood chem. Color Transp Sp Gravity pH Sugar Protein RBC WBC Cast Epith cell Bacteria Mucus th Crystals Am urates straw Clear 1.010 8.0 NEG NEG 0-1 0-2 Rare occ’l Rare Rare Urinalysis pH pCo2 po2 HCo3 o2 sat Fio2 Temp 7.408 49.1 70 31.3 93.6 21% 36.9 ABG PBS Slight poikilocytosis, acanthocytes, ovalocytes, slight toxic granulation, slight anisocytosis Table 2. Thyroid Function Tests Free T4 TSH (0.8-2.0) (0.4-6.0) 0.02 ng/dl 24.75 Uiu/ml Reference Value Result Figure 1. Electrocardiogram upon admission Table 3. Cardiac Enzymes Qualitative Troponin I CK-MB CK-ToTAl 0-6.0 21-232 PoSITIVE 1.14 543 Reference Range (mmoL) Result Figure 2. Chest radiograph on admission _______________ Corresponding author: Mary Ondinee U. Manalo, MD Department of Medicine Philippine General Hospital University of the Philippines Manila Taft Avenue, Ermita, Manila 1000 Philippines Telephone: +632 8062209 / 0923 6503548 Email: marymanalo_md@yahoo.com A Case of Chronic Diarrhea Secondary to Capillaria philippinensis in Occidental Mindoro: Possibly a Newly-Described Endemic Area? Mary Ondinee U. Manalo,1 Virgilio P. Bañez2 and Vicente Y. Belizario, Jr.3,4 1Department of Medicine, College of Medicine and Philippine General Hospital, University of the Philippines Manila 2Section of Gastroenterology, Department of Medicine, College of Medicine and Philippine General Hospital, University of the Philippines Manila 3National Institutes of Health, University of the Philippines Manila 4Department of Parasitology, College of Public Health, University of the Philippines Manila Introduction Intestinal capillariasis or capillariasis philippinensis is caused by a small nematode known as Capillaria philippinensis. Symptoms of this illness are diarrhea, borborygmi, and abdominal pain. This helminthic infection was virtually unknown until 1963 when Chitwood reported the first case, a schoolteacher from Bacarra, Ilocos Norte. He had a history of intractable diarrhea for 3 weeks with ascites, emaciation and cachexia and later died at the Philippine General Hospital in Manila.1,2 In the 1960s, a capillariasis outbreak occurred in Tagudin, Ilocos Sur where almost a hundred died.3 Another epidemic was recorded in Southern Leyte in the Philippines in the early 1980s.4 In the recent past, this parasite was also isolated in Compostela Valley Province2 and Zamboanga del Norte in Western Mindanao.5 We present a case of chronic diarrhea secondary to multiple enteric pathogens, including Capillaria philippinensis in Occidental Mindoro, a possible newly-described endemic area. Case A 41-year-old male from the town of Alacaak, Sta. Cruz, Occidental Mindoro presented with a one-year history of colicky abdominal pain and watery diarrhea. Multiple consults were done in their region that revealed “unremarkable fecalyses”. He was given various antibiotics but this did not resolve his symptoms. Six months prior to admission, four men in their barangay died from chronic diarrhea and this prompted the patient to seek consult in Manila. He was admitted in a private hospital for work-up where fecalysis again was “unremarkable”, abdominal CT that revealed no masses, and colonoscopy with biopsy that revealed mild nonspecific colitis. During this time, the patient had lost more than a third of his weight and developed bipedal edema. Patient was repeatedly readmitted but no definite diagnosis was established. He was never febrile. The patient had a history of pulmonary tuberculosis treated for only a week. He was fond of eating dogs and kilawin. He knew the four people who died in their locality. He admitted to having been in a drinking binge with at least one of them and ate kilawin during their binges. He worked as a farmer, as a fisherman, and as a tricycle driver. He would catch fish in Pagbahan River, but would sometimes buy from the local market. No other family member presented with diarrhea. He had no history of travel. The patient presented at the Emergency Room of the Philippine General Hospital severely emaciated, unable to ambulate and with palpatory BP (Figure 1). He weighed 42 kilograms (BMI=16), with bronchovesicular breath sounds, normal cardiac rate and regular rhythm, scaphoid abdomen which was normoactive, grade 2 bipedal non-pitting edema, and unremarkable digital rectal exam. Neurologic findings were normal. He was hydrated and started on inotropes. Initial investigations revealed the following: severe hypoalbuminemia (2g/L) with no proteinuria, hemoglobin 142g/L, wbc 7.4 x 109/L (neut 0.64 lymph 0.32 eos 0.013), and low electrolytes (sodium, potassium, calcium, magnesium, and phosphorus). He had normal creatinine, bilirubins, and liver enzymes. His ECG had low voltage complexes. His initial stool examination showed abundant white blood cells, without any RBC, fat globules, ova, or parasites. Fecal CASE REPORT
  • 2. Chronic Diarrhea from Capillaria philippinensis in Mindoro 82 VOL. 46 NO. 3 2012ACTA MEDICA PHILIPPINA Vol. 43 N0. 4 200912 ACTA MEDICA PHIlIPPINA Heart Failure and Short Stature in a 43 year-old male Katerina T. leyritana1 , Ma. Czarlota M. Acelajado-Valdenor1 , Amado o. Tandoc III2 and Agnes D. Mejia1 1 Department of Medicine, College of Medicine and Philippine General Hospital, University of the Philippines Manila 2 Department of Pathology, College of Medicine, University of the Philippines Manila CASE REPORT Corresponding author: Ma. Czarlota Acelajado-Valdenor, M.D. Department of Medicine Philippine General Hospital Taft Avenue, Manila, 1000 Philippines Telephone: +632 554-8488 Email: czarlota@yahoo.com Presentation of the case This is a case of a 43-year-old male presenting with short stature and heart failure. The patient was admitted at the medicine ward of the Philippine General Hospital (PGH) for dyspnea. This paper will investigate several issues: differentiating congenital from acquired hypothyroidism, the relationship between hypothyroidism and the cardiomyopathies, and the therapeutic options in patients with cardiomyopathy secondary to hypothyroidism. The patient had been born full term to a then 31-year- old Gravida 4 Para 3 (G4P3), the 4th of 9 siblings, with an apparently unremarkable delivery at home facilitated by a traditional birth attendant. He was noted to be normal at birth. The patient was allegedly at par with age both physically and mentally until eight years old when he was said to have stopped growing in height. He was brought to a private doctor, whose diagnosis was undisclosed, and he was given medications to increase height, which the patient took for only one month with no improvement. Through the years, the patient was apparently well, although still of short stature, with thick lips, coarse facial features and dry skin. He was notably slow in ambulation. He was said to have bronchial asthma at age 15 years, and since then he had been taking salbutamol tablets occasionally for bouts of dyspnea occurring one to two times annually. The patient’s symptoms started in 2001 when he was reported to have sudden loss of consciousness. During this time, the patient did not have any symptoms of heart failure; no prior seizures, cyanotic episodes, chest pain, headache, or blurring of vision. He regained consciousness shortly after and was brought to a private physician, whose assessment was a “heart problem”. He was prescribed unrecalled medications taken for a few months and eventually discontinued when the syncopal episode did not recur. In the next four years, the patient would develop intermittent, progressive exertional dyspnea and bipedal edema. later on this would be accompanied by generalized body weakness, anorexia, and constipation, severe enough to require regular laxative use. There was also a report of two more syncopal episodes. He was brought to another doctor in a private hospital where the assessment was still a “heart problem”. The patient was again prescribed unrecalled medications and again was lost to follow-up. This time, however, symptoms were persistent. He later consulted at another local hospital, where he was admitted and managed as a case of anemia and bronchial asthma. He was discharged slightly improved after four days, only to have recurrent heart failure symptoms, prompting admission at PGH. Upon admission the patient was in mild respiratory distress, with stable vital signs and no note of fever. Pertinent physical exam findings included short stature, thick lips, non- pitting periorbital edema, dry skin, a displaced apical impulse, crackles on both lung fields, and bilateral non-pitting bipedal edema. There was also a 3 cm x 3 cm reducible umbilical hernia. However, there was no pallor, no neck vein distention, no apparent congenital malformations, no cardiac murmurs and no clubbing. There was also no note of an anterior neck mass. laboratoryworkupshowedcardiomegalywithpulmonary congestion,thoracicdextroscoliosis,andatheromatousaortaby chest radiograph, and left ventricular hypertrophy by 12-lead electrocardiogram (12-l ECG) (Figures 1 and 2), normocytic normochromic anemia (Hgb 90 mg/dl), dyslipidemia, and pre-renal azotemia (serum creatinine 123 mmol). Electrolytes on admission showed slight hyponatremia, hypokalemia, and hypochloremia (serum Na 136, K 3.35, Cl 86). Blood gases revealed partially compensated metabolic alkalosis with mild hypoxemia. The patient was noted to be hypothyroid based on elevated serum thyroid-stimulating hormone (TSH) and markedly decreased serum free thyroxine (FT4). The exact values are shown in Tables 1 and 2. Upon admission to the wards, the patient was managed as having congestive heart failure from cardiomyopathy secondary to acquired hypothyroidism. oral loop diuretics, angiotensin-converting enzyme (ACE) inhibitors, beta- blockers, statins, and levothyroxine were started. Electrolyte correction was instituted. The sections of Endocrinology and Cardiovascular Diseases were co-managing the patient together with the General Medicine service. He soon developed respiratory failure, upon which the considerations were acute pulmonary congestion, nosocomial pneumonia, to rule out an acute coronary event. He was later occult blood was likewise negative. Investigations for pulmonary tuberculosis including a chest film and sputum AFB were normal. No enteric pathogen was isolated on initial stool culture. Stool was sent to the College of Public Health for FECT which revealed no parasites. A 2D-echo was requested to rule out a cardiogenic cause for the shock and it revealed a small pericardial effusion with an ejection fraction of 33%. Figure 1. Appearance of the patient prior to treatment (BMI=16 kg/m2). Since no enteric pathogen was initially isolated, the investigator initially pursued work-up for non-infectious causes like malabsorption syndromes, irritable bowel disease, malignancy, adrenal insufficiency, hyperthyroidism, and carcinoid. Infectious causes were likewise pursued. Cortisol (560 pmol/L) and thyroid function tests were both normal. Irritable bowel disease and malignancy were ruled out because of the CT scan and the colonoscopy findings. Another stool culture was done and this revealed growth of Candida species. Salmonella IgG/IgM were non-reactive. HIV screening was negative. Stool AFB was +1 on day 1 and day 2. However, the investigator was not entirely convinced that this was just TB and stool was sent almost every day for fecalysis. The patient was on inotropes and colloids during the first week of his admission. He was placed on nothing per orem, except medications, to allow time for the patient’s intestinal villi to regenerate. Gastroenterology consult was sought and the patient was treated as if he had short gut syndrome. He was started on ranitidine, loperamide, and racecadotril. Fluconazole and Category I TB treatment were started as well. He was placed on total parenteral nutrition. By the end of the second week, patient was off inotropes and was started on clear liquids. When this was tolerated, he was started on elemental feeding. However, diarrhea persisted. By the third week, serial fecalyses revealed the presence of the following: Entamoeba histolytica cysts, Strongyloides stercoralis adult and rhabditiform larvae. First line treatment for strongyloidiasis is Ivermectin but this was not available in the Philippines. Second line drug is albendazole 400 mg bid x 5 days every 2 weeks x 2 cycles and this was started on the patient the same day. Since the patient had been treated multiple times for amoebiasis, diloxanide furoate, a luminal agent, was added on top of metronidazole. The next stool sample had suspected Capillaria philippinensis ova, which were atypical because they did not possess bipolar plugs. Another stool sample was sent the following day and the diagnosis of capillariasis was established when it revealed typical Capillaria ova with bipolar plugs (Figure 2). The patient was then treated with the following drugs: albendazole 400 mg bid x 10 days then repeated after 2 weeks (this covered for both C. philippinensis and S. stercoralis); metronidazole 500 mg tabs q6 x 14 days; diloxanide furoate 500 mg tab tid x 14 days; fluconazole 200 mg cap x 10 days; and quadruple anti-Koch’s. By this time, the chronic diarrhea of the patient was attributed to: 1.) TB colitis, 2.) C. philippinensis, 3.) S. stercoralis, 4.) E. histolytica, and 5.) C. albicans. Figure 2. C. philippinensis ova recovered from the stool of the patient. Three days after being given those drugs, diarrhea resolved. A repeat 2D-Echo showed an improved ejection fraction of 72%, consistent with nutritional cardiomyopathy. After another week, the patient was discharged wheelchair- borne. He was educated on how he acquired his illness. Avoidance of eating raw fish and walking barefooted was emphasized. A month after, the patient followed up weighing 49 kg (Figure 3). He was already ambulant and had good appetite. Albumin improved from 2 g/L to 24 g/L after just one month. Repeat FECT revealed no organisms. By the time he completed his 6 months of anti-Koch’s, he was already back in Occidental Mindoro where he now drives his tricycle for a living.
  • 3. Chronic Diarrhea from Capillaria philippinensis in Mindoro 83VOL. 46 NO. 3 2012 ACTA MEDICA PHILIPPINAVol. 43 N0. 4 2009 ACTA MEDICA PHIlIPPINA 13 Heart Failure and Short Stature in a 43 year-old male transferred to the intensive care unit (ICU) for ventilatory supportandclosermonitoring.onbedsidecardiacultrasound, there was a finding of eccentric left ventricular hypertrophy, global hypokinesia with depressed overall systolic function withconcomitantspontaneousechocontrastonleftventricular (lV) cavity suggestive of rheologic stasis, the ejection fraction was 25%, with moderate mitral regurgitation, moderate aortic regurgitation with aortic sclerosis, severe tricuspid regurgitation with mild pulmonary hypertension, pulmonary regurgitation, and minimal pericardial effusion or pericardial fat pad. Cardiac enzymes were not consistent with an acute coronary event (Table 3), however, intravenous (IV) heparin (overlapping with oral warfarin) was still given to cover for the presence of a possible lV thrombus as demonstrated by rheologic stasis on cardiac ultrasound. Medications were shifted to IV diuretics and inotropes; oral digoxin was started. IV antibiotics were given for possible pulmonary infection. The patient later on showed improvement, and was eventually weaned off from ventilatory support, extubated, Table 1. Initial laboratory Results WBC RBC HGB HCT MCV MCH MCHC RDW PlT RETIC SEG lYMPH MoNo Eo BASo BlAST CBC Reference Value 5-10 4-6 120-150 0.38-0.48 80-100 Fl 27-31 PG 320-360 G/l 11.5-15.5% 200-400 0.005-0.015 50-70% 20-44% 2-9% 0-4% 0-2% 0% Result 4.5 90 0.27 Inc 48 50 2 0 0 0 RBS HGBA1C BUN CREA AlB TAG HDl lDl ToTAl CHol AST AlT Alk po4 NA K Cl CA++ P MG++ Reference Value 3.9-6.1 4.27-6.07 2.6-6.4 53-115 34-50 0.34-1.7 0.91-1.56 1.1-3.8 4.2-5.2 15-37 30-65 140-148 3.6-5.2 100-108 2.12-2.52 0.74-1 Result 6.3 6.4 5.0 123 32 0.82 0.67 4.21 5.25 95 91 184 136.9 3.35 86 2.37 2.27 0.83 Blood chem. Color Transp Sp Gravity pH Sugar Protein RBC WBC Cast Epith cell Bacteria Mucus th Crystals Am urates straw Clear 1.010 8.0 NEG NEG 0-1 0-2 Rare occ’l Rare Rare Urinalysis pH pCo2 po2 HCo3 o2 sat Fio2 Temp 7.408 49.1 70 31.3 93.6 21% 36.9 ABG PBS Slight poikilocytosis, acanthocytes, ovalocytes, slight toxic granulation, slight anisocytosis Table 2. Thyroid Function Tests Free T4 TSH (0.8-2.0) (0.4-6.0) 0.02 ng/dl 24.75 Uiu/ml Reference Value Result Figure 1. Electrocardiogram upon admission Table 3. Cardiac Enzymes Qualitative Troponin I CK-MB CK-ToTAl 0-6.0 21-232 PoSITIVE 1.14 543 Reference Range (mmoL) Result Figure 2. Chest radiograph on admission Figure 3. The patient after treatment (BMI=20 kg/m2). Discussion Capillariasis is a parasitic disease caused by infection with any of the four Capillaria species found to infect humans: Capillaria hepatica, C. aerophila, C. plica, and C. philippinensis.3 Capillaria philippinensis inhabits the small bowel of humans, causing mostly diarrhea and malabsorption. The life cycle is incompletely understood, although freshwater fish contain larvae infectious for humans and birds. The latter is an important reservoir host, especially migratory birds that could drop their feces in any body of water. Laboratory examinations document the typical findings of protein-losing enteropathy, malabsorption, and electrolyte loss. The diagnosis is established by detecting characteristic ova or larvae in the stool. In untreated patients, mortality rate is 33%, but specific anti-helminthic therapy is effective and life-saving. Infection is prevented by eating only properly cooked freshwater fish.6 C. philippinensis was first reported in 1963 in Bacarra, Ilocos Norte Province and has been endemic in that area ever since, particularly in Pudoc Lake where it was isolated.1 Since then, additional endemic foci of C. philippinensis have been identified in Southern Leyte,3 in Compostela Valley, in Southern Mindanao,2 and in Zamboanga del Norte, Western Mindanao.5 To date, this is the first reported case of intestinal capillariasis from Occidental Mindoro, an island bounded by the Mindoro Strait and the Mamburao reef (Figure 4). There are 11 barangays in Sta. Cruz, and in Alacaak, where the patient resides, there is a freshwater reservoir called the Pagbahan River where he sometimes catches fish. People here are fond of eating kilawin, which is raw fish soaked in vinegar and seasoning. The lacustrine goby or dulong (Gobiopterus lacustris) and the Philippine anchovy or bolinaw (Encrasicholina oligobranchus) are the two most common species eaten raw in their locality because they are cheap. In fact, they are sometimes called the “poorman’s fish”. However, when there is a festivity, they would sometimes use chopped and pounded milkfish (Chanos chanos) or tanigue (Acanthocybium solandri) in their kilawin. Any of these species of fishes could have been harboring the infective larvae and could have been ingested by migratory birds as the definitive host or by men as the accidental host. Figure 4. The Municipality of Sta. Cruz, Occidental Mindoro (Source: www.wikipilipinas.org, reproduced with permission). According to the patient, people living here have water- sealed toilets, although he is aware of some families using pit privies. He also attested that some people in their locality resort to open and indiscriminate defecation. Children sometimes defecate near the shoreline when they are playing and swimming. In this case, we believe that the patient may be an “indigenous case” in that he acquired his infection from his locality (rather than an “imported case”, where a patient got the infection from an already established endemic area). He had no history of travel, and there were already 4 deaths in their area attributed to diarrhea secondary to an undetermined cause. Since migratory birds are in part responsible for dissemination, the bodies of water surrounding Sta. Cruz may have been part of their usual stops. The cycle of fish eating infected feces, then man eating infected fish could have easily been perpetuated in this area because eating raw fish is a common practice. Furthermore, since open and indiscriminate defecation has been described by the patient, fish eating not just infected bird feces, but infected human feces as well, could have been part of the cycle. This case presented with diagnostic difficulties since the patient presented with almost a year of “unremarkable”
  • 4. Chronic Diarrhea from Capillaria philippinensis in Mindoro 84 VOL. 46 NO. 3 2012ACTA MEDICA PHILIPPINA Vol. 43 N0. 4 200912 ACTA MEDICA PHIlIPPINA Heart Failure and Short Stature in a 43 year-old male Katerina T. leyritana1 , Ma. Czarlota M. Acelajado-Valdenor1 , Amado o. Tandoc III2 and Agnes D. Mejia1 1 Department of Medicine, College of Medicine and Philippine General Hospital, University of the Philippines Manila 2 Department of Pathology, College of Medicine, University of the Philippines Manila CASE REPORT Corresponding author: Ma. Czarlota Acelajado-Valdenor, M.D. Department of Medicine Philippine General Hospital Taft Avenue, Manila, 1000 Philippines Telephone: +632 554-8488 Email: czarlota@yahoo.com Presentation of the case This is a case of a 43-year-old male presenting with short stature and heart failure. The patient was admitted at the medicine ward of the Philippine General Hospital (PGH) for dyspnea. This paper will investigate several issues: differentiating congenital from acquired hypothyroidism, the relationship between hypothyroidism and the cardiomyopathies, and the therapeutic options in patients with cardiomyopathy secondary to hypothyroidism. The patient had been born full term to a then 31-year- old Gravida 4 Para 3 (G4P3), the 4th of 9 siblings, with an apparently unremarkable delivery at home facilitated by a traditional birth attendant. He was noted to be normal at birth. The patient was allegedly at par with age both physically and mentally until eight years old when he was said to have stopped growing in height. He was brought to a private doctor, whose diagnosis was undisclosed, and he was given medications to increase height, which the patient took for only one month with no improvement. Through the years, the patient was apparently well, although still of short stature, with thick lips, coarse facial features and dry skin. He was notably slow in ambulation. He was said to have bronchial asthma at age 15 years, and since then he had been taking salbutamol tablets occasionally for bouts of dyspnea occurring one to two times annually. The patient’s symptoms started in 2001 when he was reported to have sudden loss of consciousness. During this time, the patient did not have any symptoms of heart failure; no prior seizures, cyanotic episodes, chest pain, headache, or blurring of vision. He regained consciousness shortly after and was brought to a private physician, whose assessment was a “heart problem”. He was prescribed unrecalled medications taken for a few months and eventually discontinued when the syncopal episode did not recur. In the next four years, the patient would develop intermittent, progressive exertional dyspnea and bipedal edema. later on this would be accompanied by generalized body weakness, anorexia, and constipation, severe enough to require regular laxative use. There was also a report of two more syncopal episodes. He was brought to another doctor in a private hospital where the assessment was still a “heart problem”. The patient was again prescribed unrecalled medications and again was lost to follow-up. This time, however, symptoms were persistent. He later consulted at another local hospital, where he was admitted and managed as a case of anemia and bronchial asthma. He was discharged slightly improved after four days, only to have recurrent heart failure symptoms, prompting admission at PGH. Upon admission the patient was in mild respiratory distress, with stable vital signs and no note of fever. Pertinent physical exam findings included short stature, thick lips, non- pitting periorbital edema, dry skin, a displaced apical impulse, crackles on both lung fields, and bilateral non-pitting bipedal edema. There was also a 3 cm x 3 cm reducible umbilical hernia. However, there was no pallor, no neck vein distention, no apparent congenital malformations, no cardiac murmurs and no clubbing. There was also no note of an anterior neck mass. laboratoryworkupshowedcardiomegalywithpulmonary congestion,thoracicdextroscoliosis,andatheromatousaortaby chest radiograph, and left ventricular hypertrophy by 12-lead electrocardiogram (12-l ECG) (Figures 1 and 2), normocytic normochromic anemia (Hgb 90 mg/dl), dyslipidemia, and pre-renal azotemia (serum creatinine 123 mmol). Electrolytes on admission showed slight hyponatremia, hypokalemia, and hypochloremia (serum Na 136, K 3.35, Cl 86). Blood gases revealed partially compensated metabolic alkalosis with mild hypoxemia. The patient was noted to be hypothyroid based on elevated serum thyroid-stimulating hormone (TSH) and markedly decreased serum free thyroxine (FT4). The exact values are shown in Tables 1 and 2. Upon admission to the wards, the patient was managed as having congestive heart failure from cardiomyopathy secondary to acquired hypothyroidism. oral loop diuretics, angiotensin-converting enzyme (ACE) inhibitors, beta- blockers, statins, and levothyroxine were started. Electrolyte correction was instituted. The sections of Endocrinology and Cardiovascular Diseases were co-managing the patient together with the General Medicine service. He soon developed respiratory failure, upon which the considerations were acute pulmonary congestion, nosocomial pneumonia, to rule out an acute coronary event. He was later laboratory results. Capillariasis could possibly be endemic in this barangay for quite some time now, but was left undiagnosed. In Compostela Valley, there have been 12 deaths before the diagnosis of capillariasis was established. This was attributed to the lack of proficiency of the local health staff in laboratory diagnosis and a general lack of awareness of this potentially fatal parasitic infection.2 An inexperienced observer may confuse the eggs with those of Trichiuris trichiura, which are larger (50 to 54 by 22 to 23 m) and barrel-shaped, with more prominent mucoid bipolar plugs.3 According to a study by Belizario et al., 54.7% of patients examined at Compostela Valley were infected with ≥1 organism, including C. philippinensis. Most of the patients were co-infected with hookworms, Endolimax nana, Entamoeba histolytica, Entamoeba coli, and Heterphyes sp.2 This is called polyparasitism, and the study done in Mindanao reflected the same problem in Thailand where it is a common practice to eat koi pla (chopped raw fish mixed with lemon juice, finely cut red onion and chili) and tab kaab (pounded raw whole fish mixed with lemon juice, finely cut red onion and chili). C. philippinensis has been identified in 25 provinces in Thailand and majority of infected patients also harbored hookworms.7,8 In addition, cases of polyparasitism with C. philippinensis have also been reported in Taiwan,9 Lao Republic,10 Egypt,11-12 Iran,13 Southern Brazil14 and Africa.15 In our patient, the chronic diarrhea could have easily been caused by C. philippinensis, S. stercoralis, and E. histolytica. All these organisms are related to poor environmental sanitation, possibly stemming from indiscriminate defecation. Our patient was unique because the Capillaria eggs only surfaced after more than 10 serial fecalyses done at our Institution. This is odd, since Capillaria infections are usually prolific. Eggs, larvae, and adults appear in great numbers in stool specimens.3 This is in contrast to S. stercoralis wherein worm load is low. In these cases, chances of finding the parasite is proportional to the number of occasions in which the stool is examined, or if available, stool should be analyzed using concentration techniques. It is also important to note that occurrence of autoinfection, or the ability of a parasite to multiply and complete one’s life cycle inside humans, is recognized only in Strongyloides stercoralis and to a lesser extent, in Capillaria philippinensis infections.16 In these two infections, complete eradication of the parasite is necessary for cure. The patient also had TB colitis, which is permissive for infection with C. philippinensis and S. stercoralis.16 Parasitic overgrowth rendered him susceptible to Candida as well. In these cases of polyparasitism, morbidity becomes additive and mortality subsequently is higher. The key then to the cure of our patient was clinching the correct diagnosis that facilitated correct treatment. Conclusion In summary, we have presented a case of intestinal capillariasis from Occidental Mindoro, left undiagnosed for more than a year in different institutions. Although capillariasis contributed to his disease, polyparasitism with Strongyloides stercoralis and Entamoeba histolytica could account for the patient’s overall condition. Presently, there is still a need to identify the possible occurrence of intestinal capillariasis in other unrecognized foci and to define its geographic distribution here and abroad. Recommendations This case was reported to the Department of Health to pursue this site as a potential area for epidemiologic investigation. Accurate diagnosis will result in the appropriate treatment and provide information and evidence as basis for the control and prevention of this potentially fatal disease in the community. __________ References 1. Chitwood MB, Valesquez C, Salazar NG. Capillaria philippinensis sp. nov. (Nematoda: Trichinellida), from the intestine of man in the Philippines. J Parasitol. 1968; 54(2):368-71. 2. Belizario VY, de Leon WU, Esparar DG, Galang JM, Fantone J, Verdadero C. Compostela Valley: a new endemic focus for Capillaria philippinensis. Southeast Asian J Trop Med Public Health. 2000; 31(3):478- 81. 3. Cross JH. Intestinal capillariasis. Clin Microbiol Rev. 1992; 5(2):120-9. 4. Cross JH, Basaca-Sevilla V. Biomedical Surveys in the Philippines. 1984; NAMRU-2 SP-47:1-117. 5. Belizario VY, G Totañes FI, de Leon WU, Migriño JR Jr, Macasaet LY. Intestinal capillariasis, Western Mindanao, the Philippines. Emerg Infect Dis. 2010; 16(4):736-8. 6. Mandell GL, Bennett JE, Dolin R. Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases, 7th ed. Philadelphia, PA: Churchill Livingstone, Elsevier; 2010. 7. Saichua P, Nithikathkul C, Kaewpitoon N. Human intestinal capillariasis in Thailand. World J Gastroenterol. 2008; 14(4):506-10 8. Benjanuwattar T, Morakote N, Somboon P, Sivasomboon B. Intestinal capillariasis: indigenous cases from Chiang Mai and Phayao provinces, Thailand. J Med Assoc Thai. 1990; 73(7):414–7. 9. Bair MJ, Hwang KP, Wang TE, et al. Clinical features of human intestinal capillariasis in Taiwan. World J Gastroenterol. 2004; 10(16):2391-3. 10. Soukhathammavong P, Sayasone S, Harimanana AN, et al. Three cases of intestinal capillariasis in Lao People’s Democratic Republic. Am J Trop Med Hyg. 2008; 79(5):735-8. 11. Austin DN, Mikhail MG, Chiodini PL, Murray-Lyon IM. Intestinal capillariasis acquired in Egypt. Eur J Gastroenterol Hepatol. 1999; 11(8):935–6. 12. El-Kadi MA, Dorrah AO, Shoukry NM. Patients with gastrointestinal complains due to enteric parasites, with reference to Entamoeba histolytica/dispar as detected by ELISA E. histolytica adhesion in stool. J Egypt Soc Parasitol. 2006; 36(1):53-64. 13. Rokni MB. The present status of human helminthic diseases in Iran. Ann Trop Med Parasitol. 2008; 102(4):283-95. 14. Toledo MJ, Paludetto AW, Moura Fde T, et al. Evaluation of enteroparasite control activities in a Kaingang community of Southern Brazil. Rev Saude Publica. 2009; 43(6):981-90. 15. Crompton DW, Tulley JJ. How much Ascariasis is there in Africa? Parasitol Today. 1987; 3(4):123-7. 16. Farthing M, Fedail S, Savioli L, Bundy DAP, Krabshuis JH. WGO Practice Guideline Management of Strongyloidiasis. 2004.