COXIELLA
COXIELLA
COXIELLA
Gram(-) coccobacilli
Agent of Q fever
When inhaled from environmental sources = cause pneumonia
Have tropism for liver – reside in macrophages and cause granulomatous hepatitis
Less common: infective endocarditis = not detected by culturing blood
COXIELLA BURNETTII
BACTERIOLOGY:
ORDER = legionellales
FAMILY= coxiellacea
GENUS= coxiella
SPECIES= C.Burnetti
Primary growth niche = alveolar macrophage where it uses type 4 secretion system like
L.Pneumophilia
Continues to multiply even after phagosome-lysosome fusion
Adapted to grow at low PH, thus resits lysosomal enzymes
In its grows cycle, coxiella has a form which is resistant to drying and other environmental
conditions like bacterial spore
These spores don’t have the same chemical composition of Bacillus or Clostridum spores but
survives in prolonged periods in environment – accounts for ability of C.Burnetti to produce
infection by aerosol inhalation from a considerable distance from the source
Highly resistant to environmental stress such as high tempreatures, osmotic pressure, UV light
Can survive standard disinfectants
Dormant small-cell variant (SCV) is resistant to extracellular stresses
The more metabolically active large-cell variant (LCV) is sensitive to environmental stresses
Q FEVER:
DIAGNOSIS:
1. Serology = high titers of antibody to Q fever antigen by complement fixation, IFA, enzyme
immunoassay procedures
2. Nucleic acid assays = PCR
TREATMENT:
SUMMARY:
Multiplies in alveolar macrophage
Resists acid and enzymes of phagolysosome
Spore-like forms survive in environment
Transmission= inhalation mostly; occasionally by ingestion
Occupational exposure in abattoirs and research facilities
Systemic infections without rash
Pneumonia and endocarditis also occur
Diagnosis is serologic
ERYSIPELOTHRIX:
E.RHUSIOPATHIAE:
Gram(+) bacilli
Pleomorphic, non-motile, non-sporulating,
Facultative intracellular pathogen
Causes swine erysipelas
Erysipeloid= Rosenbach’s disease= pseudoerysipelas = bacterial infection of disease caused by
traumatic penetration of E.Rhusiopathiae
EPIDEMIOLOGY:
Ubiquitous in nature
Found in nitrogenous substance decomposition sites
Domestic swine is the most important reservoir
Organism I shed by infected animals in feces, urine, saliva, nasal secretions
Killed by moist heat at 55 degrees for 15 mins
Infection to humans= occupational exposure
PATHOGENESIS:
Exopolysaccharide capsule can protect bacteria from host defences such as:
Opsonophagocytosis by polymorphonuclear leukocytes
Intracellular killing by macrophages
Reduced stimulation of oxidative respiratory burst = intracellular survival of bacteria in
macrophages
Neuraminidase – releases terminal sialic acid residues from glycoproteins, glycolipid and
oligosaccharides expressed on host cells
Hyaluronidase – facilitates dissemination of pathogens into tissues
Adhesive surface proteins= SpaA and P64
DIAGNOSIS:
= due to these reactions, rapid identification can be achieved with API coryne system = commercial strip
system based on biochemical reactions
Resistance to vancomycin is of clinical significance, since vancomycin is often used as empiric treatment
for gram-positive infections.