1 / 50

BARTONELLOSIS

BARTONELLOSIS. By Nonso Emegoakor. Outline. Introduction Bartonellosis (CARRION’S DISEASE) Other human bartonella infections. Introduction. Bartonella species are fastidious, facultative intracellular, slow-growing, gram-negative bacteria that cause a broad spectrum of diseases man .

harlan
Download Presentation

BARTONELLOSIS

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. BARTONELLOSIS By NonsoEmegoakor

  2. Outline • Introduction • Bartonellosis (CARRION’S DISEASE) • Other human bartonella infections

  3. Introduction • Bartonella species are fastidious, facultative intracellular, slow-growing, gram-negative bacteria that cause a broad spectrum of diseases man . • About 22 Bartonella species or subspecies have been identified • B. bacilliformis,B. quintana, B.henselae cause majority of bartonella associated human infections • Prolonged intraerythrocytic infection in animals creates a reservoir for human infections

  4. Bartonellosis • B.bacilliformis is the aetiologic agent • The dx is endemic to certain areas of the Andean regions of Peru, Columbia, and Ecuador, referred to as the "verruga zone. • Transmitted by Lutzomyiaverrucarum, a sand fly of the genus Phlebotomus. • Geographic limitation seems to be related to the environmental requirements of the vector.

  5. Bartonellosis(carrion’s dx) • Oroya fever is the initial,acute, bacteremic, systemic form of the disease • verrugaperuana is its late-onset, eruptive manifestation i.e the chronic cutaneous phase • Oroya fever majorly affects tourists and transient workers who are immunologically-naive to B. bacilliformis, • whereas most cases of verrugaperuana involve native populations in the Andes.

  6. Clinical features(oroya fever) •  The acute or hematic phase usually begins about three weeks after inoculation, typically with an insidious onset of mild fever, headache, anorexia, and malaise, lasting from several days to several weeks. • Anemia,jaundice,painlesshepatomegaly and lymphadenopathy. • The inoculum size of the organism, specific organism virulence factors, nutritional status of the host, and the host's immune response to B. bacilliformis play a role in determining severity

  7. Oroya fever is associated with a greater than 40 percent mortality if untreated. In those who recover, symptoms dissipate and anemia subsides after two to three weeks • Infectious complications are primarily superinfection with Salmonella spp, Shigella, Staphylococcus aureus, or Enterobacter spp. • The most common noninfectious problems include anasarca, neurologic manifestations, and pericardial effusion.

  8. Verrugaperuana • Red, hemangioma-like, cutaneous vascular lesions of various sizes appear either weeks to months after systemic illness. • verruga lesions have been classified into three types: miliary, nodular (subdermic), and mular • miliary lesions appear as small, round, soft, pinpoint papules that cluster in crops and are confined to the papillary dermis.

  9. Untreated, miliary lesions progress to the nodular phase with nontender, wart-like lesions that may become pedunculated. • Some lesions may be subcutaneous but become apparent on the skin surface as they push upward, making the overlying skin thin and purplish in color. • As they evolve into larger and superficial lesions, they are classified as the mular form; these lesions are highly vascular, bulbous, tend to bleed easily, and can ulcerate

  10. Verugaperuana(miliary lesions)

  11. Nodular(subdermic) lesions

  12. Mular lesion

  13. Investigation • FBC shows anemia with reticulocytosis. • Giemsa-stained blood films show typical intraerythrocytic bacilli, • blood and bone marrow cultures • Serology — Antibody tests for B. bacilliformis include an immunoblot test and indirect fluorescence antibody (IFA) test. • Biopsy may be required to confirm the diagnosis of verrugaperuana

  14. Treatment • Oroya fever • Chloramphenicol (500 mg PO/IV qid for 14 days) plus another antibiotic (-lactam preferred) or ciproflox 500mg b.d x10days • Verrugaperuana • Rifampin (10 mg/kg PO qd, to a maximum of 600 mg, for 14 days) or Streptomycin (15–20 mg/kg IM qd for 10 days) • large lesions or those interfering with function may require excision

  15. Cat scratch disease • Caused by B.henselae • Usually a self limiting illness • Two general clinical presentations,namelyTypical CSD and • atypical CSD

  16. Epidemiology • Occurs worldwide, favoring warm and humid climates. in the tropics, disease occurs year-round. • healthy cats constitute the major reservoir of B. henselae, and cat fleas (Ctenocephalidesfelis) are responsible for cat-to-cat transmission. • Acquired through contact with cat(especially kittens). • Estmated incidence in U.S. is about 10 cases/100000

  17. Pathogenesis • Inoculation of B. henselae, usually results from a cat scratch or bite • With lymphatic drainage to one or more regional lymph nodes in immunocompetent hosts, a TH1 response can result in necrotizing granulomatous lymphadenitis. • Dendritic cells, along with their associated chemokines, play a role in the host inflammatory response and granuloma formation

  18. Clinical features • The primary lesion, a small (0.3- to 1-cm) painless erythematous papule or pustule, develops at the inoculation site (usually the site of a scratch or a bite) within days to 2 weeks. • Lymphadenopathy develops 1–3 weeks after cat contact. • Affected lymph node(s) are enlarged and usually painful, sometimes have overlying erythema, and suppurate in 10–15% of cases

  19. Clinical features ctd • Some patients patients have low grade fever, malaise, and anorexia. • A smaller proportion experience weight loss and night sweats mimicking the presentation of lymphoma. • Resolution is slow, requiring weeks (for fever, pain) and months (for nodal shrinkage)

  20. Primary lesion

  21. Primary innoculation lesion

  22. Cervical lymph node

  23. Atypical catscratchdx • Extranodalor complicated disease,with or without lymphadenopathy. • Extra nodal manifestations include; neurologic involvement (encephalopathy, seizures, myelitis, radiculitis, cerebellitis, facial and other cranial or peripheral nerve palsies • PUO, myalgia, arthritis or arthralgia, osteomyelitis, tendinitis, neuralgia,

  24. Parinaud'soculoglandular syndrome • Granulomatous hepatitis/splenitis, • In immunocompetent individuals, CSD—whether typical or atypical—usually resolves without treatment and without sequelae • Lifelong immunity is the rule.

  25. Pre-auricular lymphadenopathy

  26. Diagnosis • Histopathology initially shows lymphoid hyperplasia and later demonstrates stellategranulomata with necrosis, coalescing microabscesses, and occasional multinucleated giant cells • PCR of lymph node tissue, pus, or the primary inoculation lesion is highly sensitive and specific

  27. Treatment • Typical CSD; For extensive lymphadenopathy,; Azithromycin 500mgx 1/7, then 50mg qds x4/7 • CSD Retinitis and other atypical CSD;Doxycycline 100mg x/7 and rifampin 300mg b.d x4-6 weeks

  28. Bacillary angiomatosis • Is a vascular,proliferative form of bartonella infection • Occurs primarily in immunocompromised patients, • Caused by B. henselae or B. quintana, • Characterized by neovascular proliferative lesions involving the skin and other organs.

  29. RISK FACTORS • HIV infection, CLL, Chemotherapy, organ transplant • Cat ownership, cat bites and scratches • Homelessness, low socioeconomic status, exposure to body lice

  30. Lesion sites/types • Cutaneous lesions; result equally from both • Subcut lesions; mainly from B.quintana • Osseous lesions; mainly from B.quintana • Visceral involvement(peliosis); almost exclusively from B.henselae • Neurological involvement; more of B.quintana

  31. Clinical features • Cutaneous lesions may be solitary or multiple, red, flesh coloured papules, plaques. • Plaques may ulcerate,discharge and become crusted. • verrucousgrowths, large,pendunculated or polypoidexophytic masses are also seen • Subcutaneous masses or nodules • Painful osseous lesions, most often involving long bones, may underlie cutaneous lesions and occasionally develop in their absence.

  32. Diagnosis • biopsy of lesion;shows lobular vascular proliferations composed of rounded vessels lined by variably protuberant plump endothelial cells • In addition, clusters of neutrophils, neutrophilic debris, and lymphocytes are scattered throughout the lesions, especially around eosinophilic granular aggregates. • Warthin-Starry silver staining of these aggregates reveals masses of small, dark-staining bacteria • Blood cultures may be positive, PCR of tissue specimen

  33. Nodular lesion on BA

  34. Nodular lesions

  35. 4444444444444444444444444444444444

  36. TREATMENT • Bacillary angiomatosis; • Erythromycind (500 mg PO qid for 3 months)or • Doxycycline (100 mg PO bid for 3 months) • Cryotherapy, curettage and surgical excision • Excellent prognosis,antibiotics are curative

  37. COMPLICATIONS • Disfigurement • Jaundice, biliary obstruction • G I bleeding • Laryngeal obstruction • encephalopathy

  38. Endocarditis • Bartonella sp are implicated stongly in culture negative endocarditis. • B.quintana and b.henselae are most commonly involved • Risk factors associated with B. quintanaendocarditis include homelessness, alcoholism, and body louse infestation • B. henselaeendocarditis is associated with exposure to cats. Most cases involve native rather than prosthetic valves; • Patients with B. henselaeendocarditis usually have preexisting valvulopathy, whereas B. quintana often infects normal valves

  39. Clinical features • prolonged, minimally febrile or even afebrile indolent illness, with mild nonspecific symptoms lasting weeks or months before the diagnosis is made. • Initial echocardiography may not show vegetations. • Acute, aggressive disease is rare.

  40. diagnosis • Blood cultures, even with use of special techniques (lysis centrifugation or EDTA-containing tubes), are positive in only 25% of cases—mostly those caused by B. quintana and only rarely those caused by B. henselae. • Prolonged incubation of cultures (up to 6 weeks) is required. • Serologic tests—either immunofluorescence or enzyme immunoassay—usually demonstrate high-titer IgG antibodies

  41. treatment • For Suspected Bartonellaendocarditis; Gentamicinb (1 mg/kg IV q8h for 14 days) plusdoxycycline (100 mg PO/IV bid for 6 weeksc) plusceftriaxone (2 g IV qd for 6 weeks

  42. others • B. quintana causesbacteremia in homeless people • Spectrum of infection ranges from asymptomatic infection to a febrile illness with headache, severe leg pain, and thrombocytopenia. • Also historically associated with trench fever,which was an epidermic in the trenches of WW1

  43. The human body louse (Pediculushumanuscorporis) has been identified as the vector and humans as the only known reservoir. • Chronic bacteremia is managed with Gentamicin (3 mg/kg IV qd for 14 days) plusdoxycycline (200 mg PO qd or 100 mg PO bid for 6 weeks)

  44. conclusion • Bartonella species cause a variety of human infections • Adequate clinical evaluation however results in proper management most of the times

  45. Thanks for listening

More Related