COXIELLA

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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:

 Small, gram(-) bacillus


 Too small that it can pass through filters
 Causes Q fever
 Grows intracellularly
 Initially identified as new type of Rickettsia, isolated from ticks which was able to pass through
filters = Rcikettsia Burnettii
 Most closely related to Legionella
 Previously thought to be obligate intracellular parasite, but can grow in cell-free environment
unlike rickettsia

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:

 Caused by Coxiella burnettii


 Infects some animals such as goats, sheep, cattle
 C.Burnetti is found in their birth products (placenta, amniotic fluid), urine, feces, and milk of
infected animals
 People can get infected by breathing in dust that has been contaminated by infected animal
feces, urine, milk, birth products
 Some people never get sick
 Primarily a zoonosis
 transmitted from animals to humans by inhalation rather than by arthropod bite
 its distribution is worldwide among wide range of animals = cattle sheep, goats, most associated
with transmission to humans
 C.Burnetti grows well in placental tissue and at the time of parturition it contaminates the soil
and fomites = lives there for years
 Q fever occurs in people who are exposed to infected animals or their products
 Farmers, veterinarians etc are highly exposed
 Infection results from inhalation (may occur from a distance from the site of generation of
infectious aerosols)
 Infection results from ingestion of animal products such as unpasteurized milk
 HIGH FEVER

CLINICAL ASPECTS OF Q FEVER:

 Affinity for reticuloendothelial system


 Occurs 20 days after inhalation
 No rash
 Hepatosplenomegaly and abnormal liver is common
 Chronic infection may result in endocarditis = antigenic subgroup of C.burnetti
 People with acute Q fever infection recover completely
 Pregnant women who are infected even without clinical illness = at risk for miscarriage, stillbirth,
etc

DIAGNOSIS:

1. Serology = high titers of antibody to Q fever antigen by complement fixation, IFA, enzyme
immunoassay procedures
2. Nucleic acid assays = PCR

TREATMENT:

- Infections resolve spontaneously


- Doxycycline therapy shortens duration of fever
- Vaccines may stimulate antibodies

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:

 Genus Erysipelothrix is a member of class Erysipelothrichia


 Phylum= firmicutes
 3 main species:
E.Rhusiopathiae
E.Tonsillarium
E.Inopinata

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

3 major forms of disease:

1. Localized cutaneous infection = erysipeloid is most common form of human infection


2. Diffuse cutaneous infection= blood cultures are negative
3. Systemic infection = patients with fever, bacteremia, endocarditis

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:

 Isolation of organism from skin biopsy


 Grows in routine lab culture in 7 days
 Difficult to isolate = small colony size and slow growth rates
 Catalase(-)
 Oxidase(-)
 Methyl red(-)
 Indole(-)
 Esculin(-)
 Nitrate reduction(-)
 Voges proskauer(-)
 Liquefaction of gelatin(-)

= due to these reactions, rapid identification can be achieved with API coryne system = commercial strip
system based on biochemical reactions

**PCR can also be used

TREATMENT: susceptible to penicillin but resistant to vancomycin

Resistance to vancomycin is of clinical significance, since vancomycin is often used as empiric treatment
for gram-positive infections.

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