Cirrhotic patient is exhibiting fever, leukocytosis and negative blood culture without an evident source of infection often. Could this be SIRS or culture-negative bacterial infection?
Well known, that the patient with decompensated liver cirrhosis has multiple predisposing factors and mechanisms for development of infection. In this connection the presence of fever, neutrophilic leukocytosis (or >10% immature forms) and negative blood culture without an evident source of infection in patients with decompensation cirrhosis – is this systemic inflammatory response syndrome or culture-negative bacterial infection?
Dear Alessandro! Thank you.
My question concerns all patients with cirrhosis. It not incidental point. Spontaneous bacterial peritonitis has accurate criteria.
My question was not absolutely correct. I have already corrected.
Sincerely, Zmicer
Ok. Thank You.
If the patient with decompensated cirrhosis has signs of systemic inflammatory response (fever, leukocytosis, etc.) and/or serologic markers of inflammation (CRP, procalcitonin, LBP) and negative culture of blood, AF, urine and other organic fluid, whether it is possible to name it culture-negative bacterial infection or undetermined infection?
Sincerely, Zmicer.
Hi Zmicer,
Have you tried strict anaerobic culture. There is one strict anaerobe that causes necrotic liver disease in a vide range of mammals. Clostridium novyi type A. Vets are more familiar with it as Bl;acks Disease in cattle and aero-chocolate liver in pigs. It is rather difficult to culture. In the 2000 outbreak among intravenous drug uses in the UK, Brazier was getting 40% false negatives with trhe best available technology. He declared the usual kits found in hospitals useless. The man to copntact is Dr. Jon Brazier Anaerobe Reference Laboratory NPHS Microbiology Cardiff University Hospital of Wales. There may be DNA tests these days or a chemical assay for the alpha toxin. There is quite a lot of literature because the Americans were investigating it for use as a biological weapon.
Paients with decompensated cirrhosis may have spontaneous blood infection due to increased permeability of gut mucosa, other common sources being urinary tract and the lung. Any increase in TLC should be treated as infection even if culture is negative there is high chance of progression to SIRS and septic shock.
viral infection , tuberculosis and phlebitis also maybe case of fever
I endorse Gautam Ray's comment treat as infection until confirmed otherwise. C novyi is good at penetrating gut mucosa.
As Dr. Biddulph mentioned, there are a wide variety of organisms which are extremely difficult to grow in culture. There are a variety of PCR based methods which can suggest agent invovled. Further, culturing under aerobic and anaerobic conditions with MALDI-TOF analysis may also suggest presence of a specific organism (protein ID). I think this is a major problem and would check with lab to ensure they cover all possible bacterial genus/species, ensure that there are not other means to ID organism (PCR, protein) available and as other suggested, culture more samples from different places. One thing that is often over looked is from gut. Salmonella, Enterococcus, Clostridia, Campylobacter are often selected for when on antibotics, but they may be resistant (inherantly resistant to specific drug or develop resistance). It may be difficult to culture/ID after antibiotic treatment (empirical) may be started?
Thanks for your comment! I agree. After any antibiotic treatment the identification is impossible in our settings. I think we should consider cost effectiveness in this case also.
Can you know the publications about differences in outcomes of culture-negative infections in comparison with the identified etiology cases among cirrhotic patients (others group)? Can you share your experience.
Sincerely Zmicer.
Another point to remember is the infection of the ascitic fluid itself [spontaneous bacterial peritonitis] which is quite common in decompensated chronic liver disease and may be the source of sepsis. Other less common variants called monomicrobial non neutrocytic bacterascites [earlier stage in development of SBP] and culture negative neutrocytic bacterascites [where organisms cannot be grown in culture as Dr Biddulph mentioned] also occur and can be the source of SIRS. Even fungal infections are common in late stages of the disease
I found the publication that contains the results of the higher mortality rate among cirrhotic patients with culture-positive infections. Mortality was 44.2% when the proportion of positive cultures was greater than 50%, and it was 28.8% for lower positivity rates.
Infections in Patients With Cirrhosis Increase Mortality Four-Fold and
Should Be Used in Determining Prognosis http://www.gastrojournal.org/article/S0016-5085(10)00878-4/pdf
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