Brucella and salmonella

2. Brucella and salmonella

3. ETIOLOGY • most common organisms: • Brucella abortus (cattle) • melitensis (goat/sheep) • B. suis (swine) • B. canis (dog) • These organisms are small, aerobic, non-spore-forming, nonmotile, gram-negative coccobacill

4. EPIDEMIOLOGY • Because of improved sanitation, brucellosis has become rare in industrialized countries • Brucellosis exists worldwide • especially prevalent in the Mediterranean basin, persian Gulf, Indian subcontinent, and parts of Mexico and Central and South America

5. important clue to the diagnosis: • A history of travel to endemic regions • consumption of exotic food or unpasteurized dairy ordairy products

6. PATHOGENESIS • Routes of infection: • inoculation through cuts or abrasions in the skin • inoculation of the conjunctival sac of the eye • inhalation of infectious aerosols • ingestion of contaminated meat or dairy products

7. The risk for infection : • Nutritional &immune immune status of the host • the route of inoculum • the species of Brucella • For reasons that remain unclear, B. melitensis and B. suis tend to be more virulent than B. abortus or B. canis

8. The major virulence factor for Brucella :its cell wall lipopolysaccharide • Strains containing smooth lipopolysaccharide have been demonstrated to have greater virulence and are moreresistant to killing by polymorphonuclear leukocytes • These organisms are intracellular pathogens that can survive and replicate within the mononuclear phagocytic cells (monocytes, macrophages)

9. Organisms that are not phagocytosed by the leukocytes are ingested by the macro phages and become localized within the reticuloendothelial system • they reside within the liver, spleen, lymph nodes, and bone marrow and result in granuloma • Antibodies are produced against the lipopolysaccharide and other cell wall antigens • This provides a means of diagnosis and probably has a role in long-term immunity

10. The major factor in recovery from infection :development of a cell-mediated response resulting in macrophage activation • sensitized T lymphocytes release cytokines which activatethe macrophages and enhance their intracellular killing capacity

11. CLINICAL MANIFESTATIONS • Brucellosis is a systemic illness that can be very difficult to diagnose in children without a history of animal or food exposure • Symptoms can be acute or insidious • nonspecific • beginning 2-4 wk after inoculation classic triad: • fever • arthralgia/arthritis • hepatosplenomegaly

12. Fever of Unknown Origin • abdominal pain ,diarrhea, vomit • Headache, cough, and pharyngitis • rash • night sweats, weakness • fatigue • A common constellation of symptoms in children is refusal to eat, lassitude, refusal to bear weight, and failure to thrive

13. physical findings • Hepatosplenomegaly • monoarticular arthritis of the knees and hips in children and of the sacroiliac joint in adolescents and adults • headache, mental inattention, and depression • invasion of the nervous system occurs in only about 1 % of cases

14. Neonatal and congenital infection: • transplacentally • breast milk • blood transfusions

15. DIAGNOSIS • Routine laboratory examinations of the blood are not helpful • CBC: thrombocytopenia, neutropenia, anemia, or pancytopenia • A history of exposure to animals or ingestion of unpasteurized dairy products may be more helpful • A definitive diagnosis :recovering the organisms in the blood, bone marrow, or other tissues(culture)

16. it is prudent to alert the clinical microbiology laboratory that brucellosis is suspected • Isolation of the organism still may require as long as 4 wk from a blood culture • Bone marrow cultures may be superior to blood cultures when evaluating patients with previous antimicrobial therapy

17. The serum agglutination test (SAT) is the most widely used and detects antibodies against B. abortus, B. melitensis, and B. suis • This method does not detect antibodies against B. canis because this organism lacks the smooth lipopolysaccharide • No single titer is ever diagnostic, but most patients with acute infections have titers of >1: 160

18. Low titers may be found early in the course of the llness, requiring the use of acute and convalescent sera testing to confirm the diagnosis • Because patients with active infection have both an immunoglobulin M (IgM) and an IgG response and the SAT measures the total quantity of agglutinating antibodiesthe • total quantity of IgG is measured by treatment of the serum with 2-MercaptoEthanol

19. low levels of IgM can remain in the serum for weeks to months after the infection has been treated • It is important to remember that all titers must be interpreted in light of a patient's history and physical examination

20. False-positive results • due to cross-reacting antibodies to other gram-negative organisms such as: • Yersinia enterocolitica • Francisella tularensis • Vibrio cholerae

21. false-negative results • prozone effect: results in the presence of hightiters of antibody • To avoid this issue, serum that is being tested should be diluted to ~1 : 320.

22. the enzyme immunoassay appears to be the most sensitive method for detecting Brucella antibodies but less specific as c as compared to agglutination tests • Polymerase chain reaction

23. Differential Diagnosis • tularemia • cat scratch disease • typhoid fever • fungal infections due to histoplasmosis, blastomycosis, or coccidioidomycosis • Mycobacterium tuberculosis • atypical mycobacteria • rickettsiae, and Yersinia

24. TREATMENT

26. Doxycycline +aminoglycoside: • the most useful antimicrobial agent • associated with the fewest relapses • Treatment failures :cephalosporins, due to the intracellular nature of the organism

27. key to preventing disease:prolonged treatment • Relapse is confirmed by isolationof Brucella within weeks to months after therapy • is usually not associated with antimicrobial resistance

28. Jarisch-Herxheimer-like reaction • The onset of initial antimicrobial therapy may precipitate presumably due to a large antigen load • It is rarely severe enough to require corticosteroid therapy

29. SALMONELLOSIS

30. Salmonellosis is a common and widely distributed food-borne disease • live in the intestinal tracts of warm- and cold-Blooded animals • Salmonella typhi -Salmonella typhimurium (95%) • Orally ingested salmonellae survive at the low pH of the stomach • evade the multiple defenses of the small intestine gain access to the epithelium • enter M cells -(T and B) in the underlying Peyer patches • Salmonella serotypes that are associated systemic illness enter intestinal macro phages disseminate throughout the reticuloendothelial system • non-typhoidal Salmonella:an early local inflammatory response infiltration of polymorphonuclear leukocytes into the intestinal lumen and diarrhea

33. NTS • ) • gastroenteritis of rapid onset and brief duration • Intestiintestinal inflammation • Selflimiting gastroenteritis • unable to overcome defense mechanism

34. S. typhi • systemic disease • across the epithelium- enter intestinal macro phages and disseminate throughout the reticuloendothelial system • Longer incubation period and duration of illness • in which systemic illness predominates only a small proportion of children get diarrhea

35. S. typhi • S. choleraesuis • S. paratyphi

37. Nontyphoidal Salmonellosis • Salmonellae motile, onsporulating,nonencapsulated, gramnegative Rods – aerobically- anaerobic growth • can be killed by heating to 130°F (54.4 0C) for 1 hr or 140°(60°C) for 15min • They remain viable at ambient or reduce temperatures for days and may survive for weeks in sewage, dried foodstuffs, pharmaceutical agents, and fecal material • somatic 0 antigens and flagellar H antigens

38. Typically cause gastroenteritis that is often uncomplicated • does not need treatment • can be severe in the young, the elderly, and patients with weakened immunity

40. the 2 most important serotypes for salmonellosis transmitted from animals to humans: • Salmonella Enteritidis • Salmonella Typhimurium

41. Nontyphoidal salmonellae have emerged as a major cause of bacteremiain Africa, especially among populations with high incidence of HIV infection

43. EPIDEMIOLOGY • Salmonellosis a major public health burden and represents a significant cost to society in many countries • It is estimatedthat in the USA alone an estimated 1.4 million nontyphoidal Salmonella infections occurred in 2007 • an estimated $2.5 billion cost due to lost productivity and medical treatment

44. Salmonella infections are recognized as major causes of childhood diarrheal illness • HIV infections and malnutrition in Africa, nontyphoidal Salmonella bacteremic infections have emerged as a major cause of morbidity and mortality among children and adults

45. Incidence proportional to the standards of hygiene,sanitation, availability of safe water, and food preparation practices • In the developed world, the incidence of Salmonellainfections and outbreaks has increased several-fold over the past few decades-modern practices of massfood production

46. Salmonella gastroenteritis accounts for over half of all episodes of bacterial diarrhea in the USA • incidence peaks at the extremes of ages, among young infants and the elder • use of antimicrobials in food animals • Poultry products (as a common source of salmonellosis)

47. Enteric Fever (Typhoid Fever)

48. The incubation period :usually 7-14 days • depends on the infecting dose and ranges between 3 and 30 days • The clinical presentation varies from a mild illness with lowgrade fever, malaise, and slight, dry cough to a severe clinical picture with abdominal discomfort and multiple complications