Journal of the Royal Society of Medicine Volume 84 October 1991
Blastocystis hominis complicating ulcerative colitis
T A Jeddy FRCS G H Farrington MS FRCS Kingston Hospital, Galsworthy Road, Kingston-Upon-Thames KT2 7BE Keywords: infective diarrhoea; colitis; Blastocystis hominis
In recent years Blastocystis hominis has been found to be a clinically significant pathogen in patients with abdominal pain, diarrhoea, anorexia, malaise and tenesmus 4. We describe a patient with ulcerative colitis who had a heavy colonization of Blastocystis hominis on stool analysis and whose symptoms resolved on treatment with metronidazole and surgery was postponed5'6.
Case history A 31-year-old milkman was first seen in 1985 with influenza type symptoms, diarrhoea and tenesmua. He was invesigated with sigmoidoscopy, barium enema and cplonoscopy and a diagnosis of ulcerative colitis was made and confirmed histologically. Over the next 5 years he was treated with salazopyrine, oral steroids and colifoam enemas with symptomatic control of his disease. More recently his symptoms worsened, and his bowel action increased to 10-12/day with general debility necessitating a change in his job. He was eventually referred for a total colectomy and ileostomy in view ofthe extent ofhis disease and exacerbated symptoms on conservative management. On admission, fresh stool specimens showed heavy colonization with Blastocystis hominis.
He was given a course of metronidazole with resolution of his symptoms. The frequency of bowel action reduced to 2-3/day and he went back to work. After 2 months of remission his symptoms have recurred with bowel actions up to 4-5 times per day. Repeated examinations of stool specimens were negative for Blastocystis hominis and he underwent a total colectomy with ileostomy.
623
Case presented to Clinical Section, 8 June 1990
Discussion Blastocystis hominis, a protozoan and a strict anaerobe is well recognized as a pathogen although it can exist as a normal commensal. The major symptoms consist of abdominal pain, anorexia, diarrhoea and flatulence; occasionally reported symptoms are bloody stools, nausea, general malaise, and tenesmus7. Treatment consists of a course of metronidazole 2 g daily for 5 days. The response of our patient to metronidazole therapy raises the possibility that other ulcerative colitis patients might benefit from this treatment and so postpone or avoid the need for major surgery. We would suggest the examination of stool specimens, looking specifically for this organism be performed routinely in ulcerative colitis patients with refractory symptoms. References 1 Bariari MJ. B Hominis (sic). Prensa Med Argent 1924;II:854-8 2 Caderin CC. El B Hominis como parasito. Rev Med Trop Parasitol 1937;3:207-13 3 Russo AR, et al Presumptive evidence of B hominis as cause of colitis. Arch Intern Med 1988;148:1064 4 Vannatta et aL B hominis infection presenting as recurrent diarrhoea. Ann Intern Med 1985;102:495-6 5 Ricci N, et aL B hominis a neglected cause of diarrhoea. Lancet 1984;i:966 6 Sheehan DJ, et al. Association of Blastocystis hominis with signs and symptoms of human disease. J Clin Microbiol 1986;24:548-50 7 Guglietnetti P, et al. Family outbreak of B hominis associated gastroenteritis. Lancet 1989;ii:1394
0141-0768/91/ 100623-01/$02.00/0 © 1991
The Royal Society of Medicine
Correspondence to Mr G H Farrington, Consultant Surgeon, Kingston Hospital, Galsworthy Road, Kingston-Upon-Thames KT2 7BE
(Accepted 22 May 1991)
Successful treatment of neonatal purpura fulminans with epoprostenol
history of vascular or autoimmune disease. The mother had been well throughout the pregnancy and there was no history of drug ingestion. The mother was admitted 96 hours before delivery with spontaneous rupture of the membranes. A sample of amniotic fluid was taken for culture. At the onset of spontaneous labour she was commenced on intravenous
F J Stewart MRCP1 B G McClure FRCP1 E Mayne FRCP FRCPath2 'Neonatal Unit, Royal Maternity Hospital, Belfast and 2Department of Haematology, Royal Victoria Hospital, Belfast
Case presented to Section of Paediatrics, 30 November 1990
Keywords: epoprostenol; neonate; purpura
Severe purpura occurring in the early neonatal period is a rare but serious condition which can result in substantial tissue loss. We report such a case in which the progression of lesions was initially halted and then reversed by an infusion of epoprostenol. Case report A female infant was born at 33 weeks gestation to a healthy, 29-year-old, primigravida mother. There was no family Correspondence to Dr F J Stewart, Department of Medical Genetics, Tower Block, Belfast City Hospital, Lisburn Road, Belfast BT9 7AB
2
a..:.-s.:-. i~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~..........|
Figure 1. Both feet seen shortly after infusion of epoprostenol was commenced. There is an obvious demarcation line on the right foot and discoloration of the toes on the left
0141-0768/91/ 100623-02/$02.00/0 © 1991 The Royal Society of Medicine
624
Journal of the Royal Society of Medicine Volume 84 October 1991
Table 1. Haematology results Morning (Day 1)
Prothrombin time (sec) PTTK (sec) TCT (sec) Reptilase (sec) Fibrinogen (gll) FDP (jg/ml) Protein C X-linked FDP (ng/ml) Factor VIII RAg AT III (functional)
Haemoglobin (g/dl) White blood cells x 109/1 Platelets x 109/l Reticulocytes Nucleated red blood cells
21 65 18 25 2.8 160 31% 1600 170% 39%
15.1 9.5 136
ampicillin 2 g 6 hourly. A female infant weighing 1972 g was delivered vaginally. Apgar scores were 7 at one min and 9 at 5 min. She was given intravenous vitamin K 1 mg at birth. Because of the history of prolonged rupture of the membranes and the degree of prematurity the baby was transferred to the special care baby unit. A full septic screen was carried out and the baby was commenced on intravenous penicillin and gentamicin. An initial ultrasound scan of the head was normal. By 5 hours there was a rapidly progressing vasculitis with lesions extending as far as the buttocks. There was a marked demarcation line on the feet (Figure 1). A full haematological and coagulation profile (excluding protein S) was performed. Hydrocortisone 100 mg (intravenous) was given immediately. An infusion of dextran 70 at a dose of 20 ml/kg was commenced. Antibiotic cover was changed to a combination of flucloxacillin, gentamicin and metronidazole which was felt to cover all likely pathogens known to cause similar lesions. An infusion of fresh frozen plasma 20 ml/kg was given twice daily. There was no improvement following these measures. Epoprostenol is a known vasodilator and inhibitor of platelet aggregation. One of us had seen epoprostenol used in older children with a similar clinical picture, secondary to septicaemiia, with good effect and so an infusion of epoprostenol was commenced at an infusion rate of 5 ng/kg/min and increased to 20 ng/kg/min. We did not experience major problems with hypotension. Serial ultrasound scans of the head remained normal. Haematological results are shown in Table 1. A protein C level of 31% was felt to be acceptable for a baby of this gestation and would not have accounted for the clinical findings. The results indicated that an active vasculitic process was occurring but did not reveal an underlying cause. Culture of amniotic fluid grew a streptococcus (not gp B), an anaerobic gram positive coccus and a coagulase negative staphylococcus. Apart from a coliform isolated from the gastric aspirate, all other cultures from the baby were sterile. C reactive protein was 32.3 (normal
Blastocystis hominis complicating ulcerative colitis
T A Jeddy FRCS G H Farrington MS FRCS Kingston Hospital, Galsworthy Road, Kingston-Upon-Thames KT2 7BE Keywords: infective diarrhoea; colitis; Blastocystis hominis
In recent years Blastocystis hominis has been found to be a clinically significant pathogen in patients with abdominal pain, diarrhoea, anorexia, malaise and tenesmus 4. We describe a patient with ulcerative colitis who had a heavy colonization of Blastocystis hominis on stool analysis and whose symptoms resolved on treatment with metronidazole and surgery was postponed5'6.
Case history A 31-year-old milkman was first seen in 1985 with influenza type symptoms, diarrhoea and tenesmua. He was invesigated with sigmoidoscopy, barium enema and cplonoscopy and a diagnosis of ulcerative colitis was made and confirmed histologically. Over the next 5 years he was treated with salazopyrine, oral steroids and colifoam enemas with symptomatic control of his disease. More recently his symptoms worsened, and his bowel action increased to 10-12/day with general debility necessitating a change in his job. He was eventually referred for a total colectomy and ileostomy in view ofthe extent ofhis disease and exacerbated symptoms on conservative management. On admission, fresh stool specimens showed heavy colonization with Blastocystis hominis.
He was given a course of metronidazole with resolution of his symptoms. The frequency of bowel action reduced to 2-3/day and he went back to work. After 2 months of remission his symptoms have recurred with bowel actions up to 4-5 times per day. Repeated examinations of stool specimens were negative for Blastocystis hominis and he underwent a total colectomy with ileostomy.
623
Case presented to Clinical Section, 8 June 1990
Discussion Blastocystis hominis, a protozoan and a strict anaerobe is well recognized as a pathogen although it can exist as a normal commensal. The major symptoms consist of abdominal pain, anorexia, diarrhoea and flatulence; occasionally reported symptoms are bloody stools, nausea, general malaise, and tenesmus7. Treatment consists of a course of metronidazole 2 g daily for 5 days. The response of our patient to metronidazole therapy raises the possibility that other ulcerative colitis patients might benefit from this treatment and so postpone or avoid the need for major surgery. We would suggest the examination of stool specimens, looking specifically for this organism be performed routinely in ulcerative colitis patients with refractory symptoms. References 1 Bariari MJ. B Hominis (sic). Prensa Med Argent 1924;II:854-8 2 Caderin CC. El B Hominis como parasito. Rev Med Trop Parasitol 1937;3:207-13 3 Russo AR, et al Presumptive evidence of B hominis as cause of colitis. Arch Intern Med 1988;148:1064 4 Vannatta et aL B hominis infection presenting as recurrent diarrhoea. Ann Intern Med 1985;102:495-6 5 Ricci N, et aL B hominis a neglected cause of diarrhoea. Lancet 1984;i:966 6 Sheehan DJ, et al. Association of Blastocystis hominis with signs and symptoms of human disease. J Clin Microbiol 1986;24:548-50 7 Guglietnetti P, et al. Family outbreak of B hominis associated gastroenteritis. Lancet 1989;ii:1394
0141-0768/91/ 100623-01/$02.00/0 © 1991
The Royal Society of Medicine
Correspondence to Mr G H Farrington, Consultant Surgeon, Kingston Hospital, Galsworthy Road, Kingston-Upon-Thames KT2 7BE
(Accepted 22 May 1991)
Successful treatment of neonatal purpura fulminans with epoprostenol
history of vascular or autoimmune disease. The mother had been well throughout the pregnancy and there was no history of drug ingestion. The mother was admitted 96 hours before delivery with spontaneous rupture of the membranes. A sample of amniotic fluid was taken for culture. At the onset of spontaneous labour she was commenced on intravenous
F J Stewart MRCP1 B G McClure FRCP1 E Mayne FRCP FRCPath2 'Neonatal Unit, Royal Maternity Hospital, Belfast and 2Department of Haematology, Royal Victoria Hospital, Belfast
Case presented to Section of Paediatrics, 30 November 1990
Keywords: epoprostenol; neonate; purpura
Severe purpura occurring in the early neonatal period is a rare but serious condition which can result in substantial tissue loss. We report such a case in which the progression of lesions was initially halted and then reversed by an infusion of epoprostenol. Case report A female infant was born at 33 weeks gestation to a healthy, 29-year-old, primigravida mother. There was no family Correspondence to Dr F J Stewart, Department of Medical Genetics, Tower Block, Belfast City Hospital, Lisburn Road, Belfast BT9 7AB
2
a..:.-s.:-. i~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~..........|
Figure 1. Both feet seen shortly after infusion of epoprostenol was commenced. There is an obvious demarcation line on the right foot and discoloration of the toes on the left
0141-0768/91/ 100623-02/$02.00/0 © 1991 The Royal Society of Medicine
624
Journal of the Royal Society of Medicine Volume 84 October 1991
Table 1. Haematology results Morning (Day 1)
Prothrombin time (sec) PTTK (sec) TCT (sec) Reptilase (sec) Fibrinogen (gll) FDP (jg/ml) Protein C X-linked FDP (ng/ml) Factor VIII RAg AT III (functional)
Haemoglobin (g/dl) White blood cells x 109/1 Platelets x 109/l Reticulocytes Nucleated red blood cells
21 65 18 25 2.8 160 31% 1600 170% 39%
15.1 9.5 136
ampicillin 2 g 6 hourly. A female infant weighing 1972 g was delivered vaginally. Apgar scores were 7 at one min and 9 at 5 min. She was given intravenous vitamin K 1 mg at birth. Because of the history of prolonged rupture of the membranes and the degree of prematurity the baby was transferred to the special care baby unit. A full septic screen was carried out and the baby was commenced on intravenous penicillin and gentamicin. An initial ultrasound scan of the head was normal. By 5 hours there was a rapidly progressing vasculitis with lesions extending as far as the buttocks. There was a marked demarcation line on the feet (Figure 1). A full haematological and coagulation profile (excluding protein S) was performed. Hydrocortisone 100 mg (intravenous) was given immediately. An infusion of dextran 70 at a dose of 20 ml/kg was commenced. Antibiotic cover was changed to a combination of flucloxacillin, gentamicin and metronidazole which was felt to cover all likely pathogens known to cause similar lesions. An infusion of fresh frozen plasma 20 ml/kg was given twice daily. There was no improvement following these measures. Epoprostenol is a known vasodilator and inhibitor of platelet aggregation. One of us had seen epoprostenol used in older children with a similar clinical picture, secondary to septicaemiia, with good effect and so an infusion of epoprostenol was commenced at an infusion rate of 5 ng/kg/min and increased to 20 ng/kg/min. We did not experience major problems with hypotension. Serial ultrasound scans of the head remained normal. Haematological results are shown in Table 1. A protein C level of 31% was felt to be acceptable for a baby of this gestation and would not have accounted for the clinical findings. The results indicated that an active vasculitic process was occurring but did not reveal an underlying cause. Culture of amniotic fluid grew a streptococcus (not gp B), an anaerobic gram positive coccus and a coagulase negative staphylococcus. Apart from a coliform isolated from the gastric aspirate, all other cultures from the baby were sterile. C reactive protein was 32.3 (normal
