Review of clinical and laboratory features of human brucellosis.

Infection with Brucella spp. continues to pose a human health risk globally despite strides in eradicating the disease from domestic animals. Brucellosis has been an emerging disease since the discovery of Brucella melitensis by Sir David Bruce in 1887. Although many countries have eradicated B. abortus from cattle, in some areas B. melitensis and B. suis have emerged as causes of this infection in cattle, leading to human infections. Currently B. melitensis remains the principal cause of human brucellosis worldwide including India. The recent isolation of distinct strains of Brucella from marine mammals as well as humans is an indicator of an emerging zoonotic disease. Brucellosis in endemic and non-endemic regions remains a diagnostic puzzle due to misleading non-specific manifestations and increasing unusual presentations. Fewer than 10% of human cases of brucellosis may be clinically recognized and treated or reported. Routine serological surveillance is not practiced even in Brucella - endemic countries and we suggest that this should be a part of laboratory testing coupled with a high index of clinical suspicion to improve the level of case detection. The screening of family members of index cases of acute brucellosis in an endemic area should be undertaken to pick up additional unrecognised cases. Rapid and reliable, sensitive and specific, easy to perform and automated detection systems for Brucella spp. are urgently needed to allow early diagnosis and adequate antibiotic therapy in time to decrease morbidity / mortality. The history of travel to endemic countries along with exposure to animals and exotic foods are usually critical to making the clinical diagnosis. Laboratory testing is indispensable for diagnosis. Therefore alertness of clinician and close collaboration with microbiologist are essential even in endemic areas to correctly diagnose and treat this protean human infection. Existing treatment options, largely based on experience gained > 30 years ago, are adequate but not optimal. In our experience, an initial combination therapy with a three drug-regimen followed by a two-drug regimen for at least six weeks and a combination of two drugs with a minimum of six weeks seems warranted to improve outcome in children and adult patients respectively with laboratory monitoring. A safe and effective vaccine in humans is not yet available. Prevention is dependent upon the control of the disease in animal hosts, effective heat treatment of dairy produce and hygienic precautions to prevent occupational exposure. This review compiles the experiences and diagnostic and treatment paradigms currently employed in fighting this disease.

Helicobacter pylori infection and erosive gastritis.

One hundred and eleven patients were included in the study. Thirty seven had erosive gastritis, thirty four chronic gastritis and forty were controls without any gastrointestinal diseases confirmed by symptoms and upper gastrointestinal endoscopy. Patients with erosive gastritis were divided into non-steroidal anti-inflammatory drug (NSAID) users and non-users. H pylori status was determined by urease test, serology and/or histology. The prevalence of H pylori was compared between the various groups. The prevalence of H pylori infection in erosive gastritis, chronic gastritis and controls was 68%, 76% and 65%, respectively, the difference was not significant (P > 0.05), 8 out of 11 patients with erosive gastritis and NSAID use (73%) were positive for H pylori. Likewise 17/26 patients with erosive gastritis without NSAID use (65%) were positive for H pylori (P > 0.05). Body of the stomach (65%) was the commonest site for erosions compared to antrum (43%) or fundus (27%) (P < 0.02). H pylori infection does not predispose to erosive gastritis. NSAID use does not affect H pylori prevalence. Routine H pylori eradication is, therefore, not indicated in patients with erosive gastritis infection. Body of the stomach is the most predominant site for erosions.

Helicobacter pylori infection in duodenal ulcer with gastric outlet obstruction.

One hundred and three patients were included in the study. Thirty seven had duodenal ulcer (DU) (Group I), 35 DU with gastric outlet obstruction (GOO) with presence of an active ulcer in the duodenum (Group II). Thirty one had DU with GOO but no active ulcer (Group III). Presence of H. pylori infection was determined by urease test, serology and/or histology. The prevalence of H. pylori in these groups was compared. Levels of Anti-H. pylori IgG antibody titres were also compared. The patients with duodenal ulcer (DU) were significantly younger (38 +/- 2 years) compared to those with established gastric outlet obstruction without ulcer (45 +/- 2 years) (P = 0.02). The prevalence of H. pylori infection in DU (95%), DU with GOO with ulcer (91%) and DU with GOO but no ulcer (90%) was not significantly different (p > 0.05). Anti-H. pylori IgG antibody titre levels were 72 +/- 6 EU/ml in Group III. The titre levels between Group I and Group III were significantly different (P < 0.05). The prevalence of H. pylori infection is high is patients with DU and is unaltered by gastric outlet obstruction. The presence or absence of an active ulcer with gastric outlet obstruction does not affect its association with H. pylori infection.

Clinical and laboratory profile of sixty patients with AIDS: a South Indian study.

Sixty patients who fulfilled the WHO case definition of acquired immunodeficiency syndrome (AIDS) were admitted and treated between January 1993 and June 1995 in JIPMER Hospital, Pondicherry, South India. Their mean age was 30.3 +/- 6.4 years. Male: female ratio was 5 : 1. The heterosexual route was the major mode of transmission (96.7%). Fever was the commonest presentation (98.3%), followed by weight loss (85%) and cough (36.7%). The commonest opportunistic infection seen was tuberculosis (pulmonary, extrapulmonary - single or in combination) followed by esophageal candidiasis. Cryptococcal meningitis, intestinal crytosporidiosis, CNS toxoplasmosis, Pneumocystis pneumonia and group B Salmonella septicemia were the other infections encountered. Ten out of the 38 patients with tuberculosis were followed up on antituberculous treatment for 6 months. Seven out of 18 patients with esophageal candidiasis were treated with ketoconazole.

Multiply resistant Haemophilus influenzae type b causing meningitis.

The isolation from patients of meningitis, of two multidrug resistant strains of H. influenzae is of relevance to the empirical treatment of meningitis patients. The isolates produced beta lactamase and had higher MICs as compared to the four H. influenzae strains sensitive to the drugs commonly used for the treatment of meningitis. The cephalosporins and gentamicin were found to be effective antibiotic agents. The occurrence of resistance to ampicillin, chloramphenicol, cloxacillin, cotrimoxazole, tetracycline, penicillin and erythromycin is of concern.