Fever in the returned traveller

Today in morning report we discussed a patient referred for fever.

The patient was otherwise well with no significant past medical history, not on any medications, no allergies, non-smoker. 

The patient had just returned from a trip, travelling with friends

This is a case of fever in the returned traveller.

Things to know:

   1.     Where did you go

   2.     When were you there (date arrived/left)

   3.     What did you do?

a.     Pre-travel: vaccines, pills (malaria proph).

b.     Travel: Itinterary!

                                               i.     Purpose: VFR (Visiting friends and relatives) – increased risk                   because (perhaps) less likely to seek pretravel advice, meds,                   vaccines, they lose innate immunity

                                              ii.     Urban vs rural

                                             iii.     Water: fresh/salt:

                   -   Fresh water fast moving – Lepto

                   -   Fresh water slow moving - schisto

                                             iv.     Bites

            a.     Mosquitos: malaria (Anopheles- night biters), dengue                     (Aedes- day biters), yellow fever

b.     Tic: ricketsial, lyme

c.     Sandfly (leishmaniasisi)

d.     Others include: mites, fleas (plague)

     v.   Exposures:

a.     Human: sexual

b.     Dogs/bats: rabies

c.     Other animals: goats, rodents

d.     Food: bottled water? Local

                                                                 -      Diarrheal bugs (salmonella typhi), hep A, unprocessed cheese (brucella)

   4.     Illness itself

-       Associated Symptoms

o   Retro-orbital pain: think dengue (+/- rash few days later)

o   Conjunctivitis: think leishmaniasis

o   Hematuria: think schisto

o   Resolving fever followed by terrible arthritis: Chikungunya (means “leaning forward”, because bent over with pain)

o   Rose spots, relative brady, diarrhea (sometimes constipation in adults) think typhoid

Our case:

Onset of fever 1 day before returning home. Generally unwell. Headache. 3 days later rash developed.

7 days abroad.  Water sports ie scuba. No fresh water exposure. No animal exposures. No sexual activity. Pre-travel received vaccinations for hepatitis A, yellow fever.

Diagnostic approach to FTR (Fever in the Returned Traveller): 

related infection vs unrelated infection vs not infection (ie VTE, drug fever)

Think about long incubation that may have been acquired prior to leaving OR short incubation that was acquired during trip

Influenza: short incubation period 12-48 hours

Hep A, B, C, HIV, longer incubation periods

Infections related to travel

**FTR is always malaria until proven otherwise: ie that you determine that malaria is not endemic in that area or 3x thick/thin smears negative. 

(malaria, typhoid, dengue, hep A account for ~80% of diseases from tropics)

Given the constellation of symptoms, the diagnosis here was Dengue.

Dengue

-       most common mosquito borne illness

-       SA/Caribbean, SE asia

-       Aedes mosquito (day biters)

-       Urban

-       4 types 1,2,3,4

-       Once get one type of dengue will be immune. BUT if you get dengue with a second type,       higher (though still small) chance of bad complications

-       Retroorbital pain, bone pain are classic features, rash

-       Dengue hemorrhagic fever: low plt, plasma leakage

-       Measles mimics

-       Incubation time is ~7 days (often 3-4d)…after 14 days can feel like out of the woods.

-       Supportive management

   For more on FTR see this NEJM review article

Invasive pneumococcal disease

In today’s morning report, we discussed a 72 year old female presenting with fever, cough, and headache.

PMH was significant for recurrent ovarian cancer with prior debulking, radiation therapy, and multiple courses of chemotherapy, and a Port-A-Cath in place, most recent chemo 6 weeks ago for disease recurrence. She also has a history of (truly) recurrent UTI, in part due to mass compression requiring a ureteric stent.

History reveals a 5 day history of subjective fevers, productive cough, and tension headache.

Exam was normal, no evidence of CNS infection, normal respiratory exam with no oxygen requirements, no signs of IE, and a normal abdo exam, with no flank tenderness.

DDx is infection, including

-        -sinusitis

-        -pneumonia

-        -CNS infection

-        -Urinary infection (given her personal hx and RF)

     -Line infection given her Port-A-Cath

-

Some take home points;

Fever from a GU source points to pyelo.

Fever is a very sensitive sign for pyelo, over 90% sensitive

Flank pain is INSENSITIVE.

Sinusitis can be differentiated into acute vs chronic

Acute

-        -within 4 weeks

-        -within first 7 days, 98% viral

-        -Risk of bacterial goes up after day 7

           o   S. pneumo, H. inf, moraxella

Aside: The American Academy of Family Medicine recommends (as part of the choosing wisely campaign) against empiric antibiotic therapy in patients presenting with mild to moderate sinusitis lasting less than 7-days from the start of their illness

Chronic

-       - 6 or more weeks

-        -structural abnormality

Complications of acute bacterial sinusitis are rare, but are important to consider and can be thought of as intracranial (subdural empyema, epidural abscess, brain abscess, venous sinus thrombosis, meningitis) or extracranial (orbital cellulitis, orbital abscess and subperisoteal abscess). 

Back to the case…admitted for further workup, blood cultures grew 2/2 S. pneumo. 

*Given the presence of positive cultures from a sterile site, she is considered to have invasive pneumococcal disease

S. pneumo sensitive to Penicillin for both CNS or non-CNS infections, essentially meaning MIC is low.
Rates of penicillin resistance are rising, 3rd generation cephalosporins would then be the next choice.

Strep pneumo

-        -Gram positive cocci in pairs/chains, alpha hemolytic, ENCAPSULATED

-        -Other encapsulated organisms:

      o   H.inf (Type B)

      o   Neisseria

      o   GBS

      o   Klebsiella

            o   Capnocytophagia

Clinical manifestations of S.pneumo

-        -colonized in URTI: can lead to OM, sinusitis, pneumonia,

-        -this can lead to bacteremia, CNS infection, IE, MSK (Vertebral OM)

     

     See here for more on invasive pneumococcal disease

Weak, unwell & puffy

Morning report today was about a young patient presenting with abdominal pain, but then was found to have a history of generally feeling unwell, reportedly becoming “puffier”, gaining weight, and simply not feeling well. Physical examination included normal vitals (not what we were expecting), but significant for delayed, or “hung” reflexes, nonpitting edema throughout, as well as generalized weakness.

Ultimately, investigations revealed a TSH of > 100

Hypothyroidism ranges from subclinical hypothyroidism, overt hypothyroidism, all the way to myxedema coma.

The pathogenesis all stems from the lack of intracellular T3 and lack of conversion from T4.  This leads to cardiac dysfunction including hypothermia, bradycardia, diastolic hypertension, and if severe enough hemodynamic compromise. It also results in fluid retention and vascular impermeability which leads to hyponatremia and edema respectively. In severe cases (myxedema), CNS disturbance occurs including coma.

Remember that in severe cases ie myxedema coma, always look for a precipitating factor, which is most commonly infection, but can include cardiac events, stroke, gi bleeds, and drugs/toxins (including the rare case of bok choy induced myxedema, which is due to the thyroid inhibiting effects of metabolites of uncooked bok choy).

Clues to diagnosis on labs may include an elevated CK (hypothyroid myopathy, seen in this case as well), increased cholesterol levels and elevated liver enzymes. Also keep in mind that adrenal insufficiency can often keep the company of hypothyroidism, as do other autoimmune conditions, remembering that autoimmune thyroid disease (ie Hashimoto’s) is the most common, and part of the diagnosis is looking for these antibodies.

Treatment should be aimed at treating any underyling precipitating cause, and thyroid replacement. Remember that T3 is the active form, and that in times of systemic illness there is decreased conversion from T4 (ie the sick euthyroid syndrome characterized by normal TSH, low T3, normal T4 and elevated reverse T3).

Also remember that thyroid hormone may increase cortisol excretion and can worsen underlying adrenal insufficiency, so remember to keep an eye for that as well.

See this review article on myxedma coma for more details (the above image is from this 2011 article by Vivek et. al in the Journal of Thyroid Research).