With bacterial meningitis, temperature resolution with appropriate therapy is related to
the pathogen causing the meningitis. Meningococcal meningitis defervesces quickly over one
to three days whereasHaemophilus influenzaemeningitis resolves over three to five days, and
severe pneumococcal meningitis may take a week or longer for the fever to decrease/become
afebrile. Viral causes of meningitis or encephalitis defervesce very slowly over a seven-day
period, and by monitoring the fever defervescence pattern a clinician can easily differentiate
viral meningitis/encephalitis from bacterial meningitis. Because fever defervescence patterns
may also point to complications, the astute clinician will monitor the fever pattern post
therapy, looking for an unexpected temperature spike after the patient has defervesced.
H. influenzaemeningitis, for example, defervesces after three to five days but if the patient
spikes a temperature after five days, this would suggest either a complication of the infection,
i.e., subdural empyema, or a complication of therapy, i.e., drug fever secondary to antimicrobial
therapy (1,2,5).
In patients with endocarditis, the fever defervescence pattern is also pathogen related.
Patients with SBE have fevers< 1028 F, and defervesce after a few days of effective antimicrobial
therapy. A subsequent temperature spike after the fever withStreptococcus viridansSBE has
resolved should suggest either a complication of SBE, i.e., septic emboli/infarcts, or a
complication of SBE therapy, i.e., drug fever. With S. aureusacute bacterial endocarditis
(ABE), patients initially have temperatures 1028 F [excluding SBE and intravenous drug abusers
(IVDAs)]. Patients withS. aureusendocarditis defervesce within three to five days after initiation
of effective anti-S. aureus therapy. The persistence of fever in a patient being treated
appropriately should suggest the possibility of a paravalvular/mild myocardial abscess. With
S. aureusABE, the reappearance of fever after initial defervescence should suggest a septic
complication, i.e., septic emboli/infarcts, paravalvular/myocardial abscess, or complication of
antimicrobial therapy, e.g., drug fever. Patients with enterococcal endocarditis have a fever
defervescence pattern intermediate betweenS. viridansSBE and ABE. Patients with enterococcal
endocarditis usually defervesce slowly over five days and recrudescence of fever in patients with
enterococcal endocarditis should suggest a septic complication or drug fever (1,5,21,43).
Fever defervescence patterns are also important in patients with CAP as well as
nosocomial pneumonias. In normal hosts with CAP due to typical bacterial pathogens,
i.e.,S. pneumoniae, H. influenzae,orMoraxella catarrhalis, fever resolves rapidly over the first
few days with effective treatment.S. pneumoniaeCAP has three possible fever defervescence
patterns, the first and most common is a rapid decrease in temperature similar to that found
inH. influenzae orM. catarrhalisCAP in normal hosts. The second with pneumococcal
pneumonia is that of initial defervescence followed in three to five days by a secondary rise
in fever. A secondary fever rise is a normal variant and does not indicate an infectious
complication. The third withS. pneumoniaeis found in patients with impaired humoral
immunity, i.e., patients with alcoholic cirrhosis, multiple myeloma, chronic lymphatic
leukemia (CLL), etc. With patients with impaired B-lymphocyte function, the fever slowly
remits during the first week of therapy. Patients with overwhelming pneumococcal sepsis,
with no humoral immunity, i.e., asplenia, remain febrile and critically ill until the infection
resolves or there is a fatal outcome.
Patients with nosocomial pneumonias NP/VAP may have temperature elevations that
are above/below 102 8 F, and fever is not a way to rule in or rule out the diagnosis of
nosocomial pneumonia. The NP/VAP is an imprecise diagnosis and is routinely given to most
patients in the CCU who have fever, leukocytosis, and pulmonary infiltrates. Therefore, most
patients who have a working diagnosis of NP/VAP in fact do not have NP/VAP but have
infiltrates, fever, and leukocytosis due to other causes. Patients being treated appropriately
with monotherapy or combination therapy for NP/VAP defervesce rapidly if the infiltrates do
in fact represent NP/VAP (5,47–50).
Monotherapy or combination therapy for NP/VAP should be with at least one agent that
has a high degree of anti-Pseudomonas aeruginosaactivity. Patients with bona fide NP/VAP
defervesce quickly within a week. The persistence of fever, i.e., lack of a fever defervescence
pattern in patients with NP/VAP suggests two possibilities, firstly, the patient has a
noninfectious disorder that is mimicking NP/VAP and for this reason is not responding to
antimicrobial therapy. Secondly, the patient could have an infectious disease, a process that is
14 Cunha