Objectives: To determine the prevalence and trends of human hookworm infection (HWI) in the Northern Territory over the past 10 years, and to assess the influence of the community children's deworming program (CCDP). Design, patients and setting: A retrospective observational analysis of consecutive microbiologically confirmed cases of HWI in patients diagnosed at NT government health care facilities and the main private laboratory servicing the NT between January 2002 and July 2012. Main outcome measures: Annual prevalence of HWI (2002–2011); age, sex, Indigenous status, residence, haemoglobin level and eosinophil count of patients with HWI; and proportion of patients within the CCDP target population (children aged 6 months to 16 years, who should receive 6‐monthly albendazole). Results: From 64 691 faecal samples examined during the study period, hookworm was detected in 112 patients. There was a downward trend in the annual prevalence of HWI, falling from 14.0 cases per 100 000 population (95% CI, 8.8–19.2) in 2002 to 2.2 per 100 000 population (95% CI, 0.3–4.1) in 2011. Only 16 patients (14.3%) fell within the CCDP target population. Seventy‐one patients (63.4%) were living in remote communities, and 94 (84.7%) were recorded as Indigenous Australians. Conclusions: The prevalence of HWI in the NT reduced over the 10‐year period. HWI predominantly occurs in individuals outside the CCDP target population. Our data support continuation of the CCDP in conjunction with improvements in housing, health hardware and health promotion. Continued use of albendazole in individuals beyond the CCDP may facilitate the eventual eradication of HWI from the NT.
T. trichiura is the most frequently identified soil-transmitted helminth infecting patients in NT Government health care facilities. Cases are identified predominantly in Indigenous patients in remote communities. We have observed a declining prevalence of whipworm infection in the NT.
A case of lung involvement with Balantidium coli complicated by severe pulmonary haemorrhage resulting in iron deficiency anaemia has not, to our knowledge, been described previously.A previously well 20-year-old white man presented to his general practitioner complaining of a gradual deterioration in his effort tolerance over the preceding month. He was pale, and a blood count showed haemoglobin (Hb) of 9.2 g/dl, a mean corpuscular volume (MCV) of 77.8 fl and platelet count of 345 x 10 9 /l; the other red and white cell indices were normal. Iron studies showed a reduced serum iron level of 3.8 µmol/l (normal 11.6 -31.3 µmol/l), transferrin 3.5 g/l (normal 2.2 -3.7 g/l), iron saturation 4% (normal 20 -50%) and ferritin 57 ng/ml (normal 20 -250 ng/ml). Serum folate and vitamin B 12 levels were normal. Iron replacement therapy was commenced per os, and the patient was referred to a surgeon with a diagnosis of iron deficiency anaemia secondary to putative gastrointestinal bleeding.The patient was admitted to hospital 3 days later after mild haemoptysis. The Hb had decreased to 6.6 g/dl and MCV to 74 fl. The international normalised ratio (INR) was 1.4. Urea and electrolytes, creatinine, liver functions, thyroid stimulating hormone, brain natriuretic peptide (pro-BNP) and alpha-1-antitrypsin were normal. A semi-quantitative procalcitonin determination showed a mildly elevated level of 0.5 -1.99 ng/ml (BRAHMS PCT-Q rapid assay). HIV and rheumatoid factor were negative. He gave no history of diarrhoea, abdominal pain or haemoptysis before admission. Dark green/black stools for the preceding few days appeared to be related to his iron replacement therapy. He was hypoxic, but the oxygen saturation improved from 45% to 92% on 40% oxygen administered via a face mask. A sinus tachycardia of 120/min and a loud S3 gallop were present. The jugular vein pressure was not elevated. Chest X-ray showed extensive bilateral alveolar infiltrates (Fig. 1). Respiratory crackles were present bilaterally on auscultation. Gastroscopy was normal, and tests for faecal occult blood were negative.His respiratory status deteriorated and he was transferred to the intensive care unit, but was not intubated. A low arterial PO 2 with normal PCO 2 , compatible with Type 1 respiratory failure, improved on Bi-pap with 40% oxygen. The echocardiograph revealed normal left ventricular function with no significant valvular disease.Blood and sputum were collected and empiric broadspectrum antibiotic and intravenous steroid therapy was initiated. Despite a blood transfusion, his respiratory status and chest X-rays showed deterioration. Sputum samples were blood-stained, but negative for acid-fast bacilli and Pneumocystis jiroveci, and only mixed oral flora were cultured. Mycoplasma pneumoniae serology testing was negative. Although the anti-nuclear factor was positive (titre 1/160), the rheumatoid factor and extractable nuclear antibody screening tests were negative, while basement membrane antibodies and neutrophil cytoplasmic antibodies were not detected...
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