Bartonella and Haemophilus Infections

Bartonella (Rochalimaea)

Four types:

(1) quintana: agent of trench fever, bacillary angiomatosis (BA), endocarditis, bacteremia; louse-borne, BPH

(2) henselae: agent of cat scratch disease (CSD) Þ BA in immunocompromised patients; fever, sepsis, endocarditis, bacillary peliosis hepatis (BPH)

(3) vinsonii: ‘vole agent’; unknown pathogenicity; never isolated from human

(4) elizabethae: isolated from blood of immunocompromised patients with endocarditis

Trench Fever: fever (five day relapsing) and non-specific symptoms (chills, headache); vectored by body louse

Cat Scratch Disease: febrile illness with localized lymphadenitis in immunocompetent hosts

four criteria for diagnosis:

(1) history of animal contact (it is a zoonosis infection)

(2) positive cat scratch skin test

(3) negative lab studies for other causes of lymphadenopathy

(4) characteristic histopathology Þ + Warthin-Starry silver stain

pathogenesis: lymphadenitis, follicular hyperplasia, stellate subcapsular necrotizing granulomas with central PMNs and palisading histiocytes

Bacillary Angiomatosis (BA): cutaneous angiogenic lesions in skin and visceral organs

seen in immunocompromised hosts, esp. HIV patients (basically CSD in immunocompromised patients)
associated with both henselae and quintana
enters body through scratch (often animal contact) or mucus membranes or conjunctivae
pathogenesis: circumscribed lesion with lobular capillary proliferation characterized by round open vessels, histiocytes, PMNs

Bacillary Peliosis Hepatis (BPH): cystic, blood-filled spaces in hepatic parenchyma and spleen

seen in immunocompromised hosts (HIV, severe wasting); associated with drugs such as anabolic steroids
associated with quintana and henselae

Immunology

acute and chronic inflammation with PMNs, mononuclear infiltrates and granuloma formation
intracellular organisms seen on tissue sections
Ab response demonstrated by indirect fluorescent antibody tests
delayed hypersensitivity skin test reactivity to antigen prepared from infected tissue

Microbiology: pleomorphic gram negative rods (with modified Brown-Hopps stain)

positive Warthin Starry silver stain; non-motile; grows in 5% CO₂ with high humidity
negative for: oxidase, urease, indole, glucose, esculin hydrolysis, nitrate reduction analysis

Treatment: erythromycin, tetracycline (stuff that gets into WBC very well); data is currently unclear

Haemophilus Influenzae

Non typable (unencapsulated): normal flora of upper respiratory tract; can cause mild mucosal URI (bronchitis, otitis media, sinusitis); rarely serious infections

Type b (Hib): serious systemic infections from bloodstream invasion; mosly in children 6-12 mos. (uncommon if >6-7 yrs old)

may be localized to meningitis: starts as URI Þ subdural effusions, tense fontanelle; seizures; only 70% of smears are positive; epiglotitis: lethal via airway obstruction; bacteremia extremely common; may have evidence of other septic foci; septic arthritis; pneumonia; periorbital cellulitis,

Types a, c, d, e, f: uncommon causes of disease; infection is sign of immunoincompetence

Epidemiology:

nontypable strains are normal flora
type b: spread by contact with infected respiratory secretions
normal colonization in children (nasopharynx) is 5%; can be as high as 50-100% in daycare
conjugate vaccines are providing herd immunity by eliminating nasopharyngeal carrier state

Pathogenesis:

nontypable: adherence; resistance to mucosal defenses
Type b: attachment and invasion through respiratory epithelium; dissemination via bloodstream; invasion into local sites (meninges - 10⁴ per ml leads to infection, joints, soft tissues)
resistance to host defenses mostly through polysaccharide capsule - PRP (polyribosyl-ribitol-phosphate)

PRP is the immunogenic component of Hib vaccines

Immunology: main host defenses are through bactericidal and opsonic activity against Type B capsular polysaccharide

IgG is cidal and opsonic; IgM is cidal but not opsonic; IgA is neither
Hib is resistant to the alternative complement pathway
Ab response to PRP is T-independent, no memory, no booster response, no response in kids <18-24 mos.
immunity against nontypable strains is from mucosal immunity
Hib vaccine (PRP) is often tied to other vaccines (diptheria, tetanus) in commercial preparations

Treatment: non-typable are often beta-lactamase positive; many antibiotics still work

Type b: almost always requires IV antibiotics; must use those which penetrate the blood-brain barrier because of possibility meningitis; need to do susceptibility tests, but third gen. cephalosporins are empiric therapy

Microbiology: pleomorphic gram negative coccobacillus

growth factors: Factor X is heat stable; Factor V is heat labile – both released from lysed RBCs
optimal growth is in 5-10% CO₂ on chocolate agar