Infectious Diseases Lessons

We had a nice citiwide presentation today.

A 7 year old healthy kid, who fell on his ankle and had a puncture wound develops a pain in his knee, with difficulty walking, more or less sub-acute presentation. the differential diagnosis included the slow growing pathogen such as atypical mycobacteria, no cardia , and molds as well as regular bacteria less potential.

MRI patella: showed osteomyelitis and grew CapnoCytophaga (grew only on chocolate plate) the human form: oxidase and catalase negative. I was surprised to learn that they secrete beta-lactamases, and more shocke to find that Clindamycin and Linezolid are an option.

We had a presentation today:

A gentleman who is a ‘tree’ surgeon, who after having an IV placed in the hospital dor TURP, develops a skin lesion, that progressively became vesicular, ulcerated and got enlarged, a biopsy showed granuloma, and he was treated with local steroids and he is already immunosuppressed from chronic oral steroids which made it much worse all over his hand.

A biopsy and culture showed our Algae: Prothoteca!

A rare organism that infected after inoculation of the skin, causes:

1-Chronic Skin infection

2-Bursitis

3-Disseminated infection.

Therapy is combination surgery and Ampho B or po azoles.

CC: neck mass
HPI: 16yo female, presented in July with a 2 month history of a slowly enlarging left neck mass. Began as a “pea-sized”
painless lump at left mandibular angle. No preceding illness. Lump has slowly enlarged and become painful. She has
had no rash, no fever, no emesis, no diarrheal illness, no neck trauma. There has been no pustule, vesicle, or drainage
from the mass. She has had an unintentional 23lb weight loss over 3 months.
Presented late in illness to her PCp, failed -10 days of cephalexin and was referred to ENT She underwent a limited
infectious workup, CT of neck and was transitioned to clindamycin. She was ultimately scheduled for elective lymph
node biopsy and exploratory dissection after worsening pain and swelling following 10 days of clindamycin. The mass
was now painful, firm, and r4cm along the left submandibular border.
Upon opening the neck, the tissue was found to be markedly fibrotic. When dissecting around the SCM, purulent
drainage was noted. No enlarged lymph nodes were found but dissection was limited secondary to the fibrotic nature of the musculature and soft tissue in the neck space. Samples of the pus were taken, and she was admitted for further  workup, placed on empiric vancomycin, metronidazole, and cefotaxime. ID was consulted at this time.
ROS: 23lb weight loss, cough, rhinorrhea x 2 weeks; Denies emesis, diarrhea, abd pain, rash
PMHx: hepatic laceration in setting of physical abuse 2008, mild intermittent asthma
Immunizations: UTO
FHx: asthma, environmental allergies, DM, HTN, kidney disease, thyroid disease; no childhood deaths
Sllx: lives in Houston, apartment; rising 11th grader
Exposures/Risks: denies IVD, no EtOH, sexually active w/ J partner, occasional condom use; got “in-home” tattoos
on wrists 02IIO by friend who “used fresh needles”; exposure kittens - 1.5months prior, no known scratches; relative
who had been imprisoned stayed in the home -2 months pior. Travel History: none
Exam: Vitals: l’ 96.8°F HR: 72 RR: 22 BP: 137/88 W1′ 55-3kg:Gen…:awake, alert, pleasant: HEENT: L neck fullness
along mandibular angle to submental region, tender to palpation, indurated/firm on palpation, pain with ranging,
swallowing: oropharynx with grade I tonsils bilaterally, mildly erythematous, no exudate: CVIRESP: RRR, no MRG:
CTAB: Lymph Nodes: left neck fullness, dressed; pre-op exam reported with T4cm indurated painful mass from left
mand;hnlar angle extending anteriorly along jawHne: Abd: soft, non-tender, n”.n:distended, no HSM: MSK/E>L: full
ROM, no painful, erythematous, swollen joints; Neuro: CN’s grossly intact, DTRs symmetric, strength; Skin..: no rash,
cursive initials 4×5Cm) on anterior wrists bilaterally with excellent penmanship
Labs: B. Henselae IgG/M = neg: EBVVCA IgM = neg: EBVVCA IgG & EBNA = pas: PPO = negative
N: 53,8% (ANC:5,5K). Hb 10.3, plt 194, cr 0.7

Imaging: CXR WNL: CT Neck (7-22):manding and reticulation of the subcutaneous fat, platysma! thickening, ~>
several enlarged enhancing nodes up to J.5cm in the left submandibular region; mild circumferential tonsillar
hypertrophy; no osseous abnormality; no periodontal diseas(:; no abscess or drainable fluid

REFER ENe ES I. Clin Microbial Infect 2003;9:881-885
2. Southern Medical Journal 2008. 101(10): 1019-1023
3. Am J Obst- Gynecol 1999;180:256-269

4. Human Pathology 1973;4:319-3305.

5.Clin Infect Dis 2003; 37;490-497
6. Indian J Med Microbiol. 2007 Oct;25(4)413-5
7. J Antimicrob Chemo 2005;56:407-409

Diagnosis: Actinomycosis

We had 2 good cases today:

1-An adult case of patient who presented with chronic symptoms of:

• Cough, non-productive
• Fever
• Night sweats
• Myalgias
• Arthralgias

History of travel in many endemic areas, desert, mexico, AZ and california

Patient got worse despite broad spectrum abx with high fever, alveolar infiltrates…and got intubated.

Negative Culture Bilateral Pneumonia:

• Auto-immune diseases: Rheumatoid lung, Wegner’s, Churg and Strauss and other rheumatological diseases (This lady had myalgias, arthralgias chronically and high CK= dermatomyositis)  You can ask for help from Rheumatology in doing the work-up or think of it and look it up yourself and impress some people.
• Cryptogenic organizing pneumonia
• Disseminated Cancers
• others…

2- A 17 year old hispanic kid with h/o “otitis” who received multiple antibiotics courses comes for fever, ‘holding his head’, neck discomfort and an LP showed: lymphocytic meningitis with low glucose, high protein.

Differential diagnosis:

First name the syndrome: Meningitis or para-meningeal focus or epidural abscess

Second: Infectious v/s non-infectious etiologies

The differential was poorly organized by one of our fellows but mostly: TB and Fungal! (low sugar, high protein)

Culture-negative meningitis–> Needs to search for Urgent Treatable Etiologies:

1. Bacterial:
   1. Partially treated bacterial meningitis
   2. Listeria can mimick lymphocytic! not to be forgotten
   3. Bacterias that do not grow easily: TB! and NTMB –> PPD, Quantiferon-Gold, MRI of the brain (lepto-meningeal enhancement)
   4. Rickettsioses et al: RMSF
   5. Treponemas: Lyme and Syphillis
2. Viral:
   1. HSV: can not miss because it is treatable (MRI is also helpful)
   2. HIV: not to miss also
   3. Immune deficient: CMV, HHV 6
3. Fungal: yeast and yeast-like, molds
   1. PCP
   2. Cryptococcus
   3. Endemic mycoses
   4. Fungi-like
   5. Molds
4. parasitics:
   1. Malaria
   2. Neurocysticercosis
   3. Toxoplasmnosis
   4. Parasitices and worms
   5. Naegelria and other amebas

Non-infectious etiologies: ask for neuro help

• Auto-immune diseases: SLE
• Granulomatous: Sarcoidosis, Behcet’s dz
• Carcinomatosis
• etc…

They presented a patient with HIV who gets an RPR of 32 and it happens that we know that RPR was negative 1 year ago, patient also had a rash.

Diagnosis and therapy:

-Therapy for patient less than 1 year for non-HIV: One injection of long acting Penicillin

-Therapy for unknown duration or > 1 year: 3 injections week apart.

-Neurosyphillis: IV Penicillin or IM penicillin with probenecid.

Should we LP?

In HIV, especially with CD 4 < 50: The stages can be skipped, Syphillis can be more agressive. The rules may not apply.

We did get reminded that an Oral Ulcer can be due to Syphillis and monitoring RPR on HIV patient routinely with other labs is wise and warranted.

We had 2 presentations today:

1- An HIV patient with lymphoma, getting chemotherpy, with AST/ALT in thousands and Total bil 7. Patient known HBV carrier.

We discussed Acute Hepatitis in HIV and specifically co-infection HBV/HIV. The principle is when you are treating HBV, you will need to treat HIV at the same time: Truvada being the common denominator. The classic issue is forgetting the HBV and switching HIV regimen by eliminating truvada which triggers a nasty hepatitis B flare.

This man in addition of having HART without HBV target is getting more immunocompromised with aggressive chemotherapy.

The question came as routine: Shouldn’t we treat Hepatitis B when we are ready to destroy the immune system because of CA or Transplant. The Answer is: YES but some forget!

The classic disaster comes with patient on Truvada and failing or getting renal failure, so the classic approach is to drop the Truvada and switch to Epzicom!! If you have HBV underlying this–> Flare of Hepatitis B.

So the differential diagnosis of Acute Hepatitis in HIV:

1- Classic Hepatitis viruses, flares, new infections

2- Drug toxicity/or toxicity from withdrawal

3-Opportunistic infections (CMV) and Cancer related to HIV

The second presentation also intresting:

Patient comes after a minimal trauma to his lower extremity with severe leg pain and swelling, toxic looking with minimal local findings–> Must recognize early necrotizing fascitis and get urgent surgery evaluation.

As a reminder: CPK can be helpful, CT Scan of the limb is also helpful. The most important this man got immediate CT Scan showing the fascitis, and surgery was done immediately that showed the severe underlying necrosis and the limb was saved. Patient had contact with cats.

The organisms cultured: Strep Group C, viridans, Prevotella and Pasteurella canis!

This remind us that: Suspect this immediately, act fast, treat very broadly until final results are back.

When in doubt go with the triad: Cefepime/Vanc/Flagyl.

Strongy again:

1- First case Strongy: I missed, patient got GI complaints, after transpant, then bilateral infiltrates (DAH) and petechial rash.

2nd case: we heard about it in Citywide, AIDS patient with diarrhea with a ‘rash’ again.

3rd case: Patient with leukemia, gets ESBL E. Coli bacteremia and meningitis each time he gets chemotherapy,  he end up having GI complaints, bowel obstruction, not getting better, neutropenic typhlitis but this time I did think about it, and gave Ivermectin, but he did not get better, diagnosis obtained pos-mortem.

They presented a case today of a patient with ALL, started getting chemotherapy and developed rapidly progressing black necrotic skin surrounded with cellulitis: necrotizing cellulitis.

1- Cutaneous Mucormycosis: classic presentation. It can happen  also after a trauma (even near drowning), burn spots and acts as nec fascitis even in immunocompetent patients (locally immunocompromised)

2-Other diferential:

Classically other molds: Aspergillosis, Fusarium etc…

Bacterias: like gram negative and PA can do the same.

As well as other causes of nec fascitis: Clostridium, SA, Strep, Anthrax, Vibrio vulnificus…

We had a pharmacology lecture today about Quinolones and Aminoglycosides:

Reminded us that FQ has low level in the blood and to be avoided in bacteremia by themselves.

Moxifloxacin only secreted at 20% in urine, more for Levaquin and less for Cipro. Absorption of Cipro: 70% or so, but Levofloxacin and Moxifloxacin > 95%.

The MIC to be considered as susceptible for serious infections are only 0.2 to have AUC/MIC above 100

Aminoglycosides have poor penetration in the tissues, especially in acidic environment

Side effects of FQ: tendinopathy, CNS and also the QT prolongation especially to be avoided with Amiodarone and other medications that potentiate the cardiac toxicity: It happened I am reading an article: called Toxic combination, a patient comes to the hospital for cardiac arrythmias because Levaquin was added for COPD exacerbation and he is on Amiodarone for A fib.

Peak/MIC determines efficacy and should be around 10 –> MIC of 1 for Gent/Tobra and MIC of 2 for Amikacin.

Our HIV meeting had 2 cases:

1-Patient with CD 4 of 330 , VL 100.000

What to give. Still drinking, using drugs.

Review of new guidelines

2-Another complicated case with HIV:

Has underlying CKD because of diabetes, HTN and underlying CAD s/p PTCA.

Treatment options.

Two intresting cases:

1-Achromobacter xylosidans

2-Strongy in AIDS

There are 2 websites very valuable:

MD Travel Health and Fit for travel

Fir for travel website has more conservative approach to Malaria and has detailed map of Malaria areas, not like the CDC.

Travel Medicine includes education, medications and vaccines:

1- Traveler’s diarrhea ,  Typhoid fever and hepatitis A:

Educate about the danger of eating local food…

Preventive medication: Rifaximin po, Typhoid fever vaccine (oral form: 4 tabs 1 qod, and injectable) and Hep A vaccine

and if the traveler got sick with fever, blood stools then Rec to treat with Levaquin 1 tab po qd x 3 days.

I was reminded by Dr. Ericsson that Rifaximin can prevent most bacterias but can not TREAT invasive diseases.

2- Malaria risks:

Preventing mosquitos is the major issue with DEET insect repelllants. He also reminded me that Mosquitos may cause Dengue: and there is no medication for this.

Malaria prophylaxis with Malarone or other agents.

In addition: Dr. E reminded me that you need to avoid ticks exposure as well–> Rickettsioses

3- Routine Vaccines such as Hep B, dT vaccine.

4-Jet lag: Ambien CR or other hypnotics (lunesta)

5- Diamox for high altitude travel

6-General recommendations: protected sex and avoid walking bare foot on beaches…

7-Other vaccines sch as yellow Fever and Japanese encephalitis as per destination.

8-DVT prophylaxis with stockings

We  had an intersting presentation in citiwide:

9 year old HM comes 1 week of sore throat, decrease intake, fatigue. Got Amoxicillin with no improvement, developped jaundice and fever, then started vomiting and became distended.

ROS: Fever, decreased activity

Myalgias, jaundice and maculo-papular rash

No suspicious contacts, pets, travel…

Physical Exam:

T 102.9 F

Jaundiced, ill-appearing

Abdomen: Hepatosplenomegaly, distended, non tender, liver 7 cm below right costal margin, palpable spleen tip.

Skin: maculopapular rash on back and shoulders

Labs:

WBC 8.1 (N 59, L 37, AL3, M2)

h/h 10.6/30.2

Plt 140–>95

Chem:

AST 736, ALT 274,  TB 7.2, DB 4.7, AP 359

INR 2.48, PTT 54.3

The LDH was very elevated, Trig was elevated….

Further Work-up: BM shows Haemophagocytic syndrome due to EBV

Nice review from CDC

A 50 year old male with no prior medical history presented for sudden onset of cough and hemoptysis, progressed very rapidly and died,  he had diffuse alveolar hemorrhage due to necrotizing pneumonia due to CA-PA. He had pancytopenia with ANC = 0, total wbc 0.4, Plt 20,000. He was in shock and DIC, ARF.

He was thought to have Hantavirus pulmonary syndrome originally! and did not have the routine w/u with blood cultures and sputum analysis.

So my differential was broad, I based on putting my MDA Anderson hat because of the neutropenia, thinking possible leukemia or AIDS underying it.

The trick is “hemoptysis” and “alveolar hemorrhage” and “immune compromise” and COPD!

Severe pneumonia with hemoptysis–> Think necrotizing pneumonia

I went into the differential of pneumonia: Bacterial/Viral/Fungal/Parasitic and non-infectious:

1- Bacterial:

• CAP: Strep pneumoniae, Atypicals: Legionella
• Gram positives: Strep A in case of Influenza, MRSA
• Gram negatives: Klebsiella! and PA from community (in COPD and AIDS)
• TB or NTMB
• Nocardia usually not acute
• Burkholderia (in asia)

2- Viral:

• Influenza (think Tamiflu) that may predispose for gram negatives and MRSA superinfections
• HSV/VZV/CMV
• Adenovirus
• Hantavirus (pneumnia+renal failure+shock): should have hemoconcentration

3- Fungal:

• Endemic mycoses
• Opportunistic fungi
• PCP and Crypto usually not hemorrhagic

4-Parasitic:

• Disseminated Strongy–> gram negative pneumonias and alveolar hemorrhage (in this case no GI issues or skin petechial rash)

Non-infectious etiologies:

• Good-pasture
• Wegner’s
• Churg and Strauss
• others…

Learning lessons:

1- Hemoptysis + pneumonia = severe = necrotizing pneumonia (think beyond CAP- CTX will not cut it)

Think PE (septic emboli)

2- Remember Smoking history is not only for IM and Pulmonary –> causes ‘local’ (lung) immune compromise: they may have on COPD bullae like TB scarring: gram negative/SA and molds superimposed infection.

Remember the case with MRSA/PA pneumonia who had TB at the same time in LBJ ICU.

3- Severe pneumonia - Think underlying immune compromise (locally) or systemically or worms bringing stuff (strongy, loeffler syndrome, lung fluke)

4- More tricks: patient had renal failure:

• Do not underdose medications: the first dose is a loading dose, then you adjust for renal failure.
• In this case: Starting Doripenem or Meropenem, consider even higher first dose
• Vancomycin the same story: I would load with 15 mg/kg then adjust as per renal failure
• In hemoptysing pneumonia: start aggressive therapy and work-up: blood cultures, sputum for gram stain, cultures, AFB and fungal cultures. Get Pulmonary and recommend bronchoscopy.  Do not forget you nasal viral cultures. Consider Galactomannan, and beta-glucan levels. Do not hesitate to start in severe pneumonia: Tamiflu that may underlie your SA/PA/Fungal. Get your urine Crypto/histo if needed. Get your Strep pneumo and Legionella
• Consider Bioterrorism: Anthrax, Tularemia/pestis
• Put your MDA hat: treat fast, act fast

I keep getting the same issue.

Patient comes for Crypto meningitis, we start Ampho B deoxycholate and patient keeps spiking fevers:

1- Is it Crypto not getting better?

2- Is it a disease not getting treated

OR

3- Just Ampho B deoxycholate side effect! drug fever?

A 4 year old boy that got admitted after near-drowning, and got bilateral pneumonia, was not getting better on Cefepime and Vanc.

Differential:

-MDR organisms (PA, acinetobacter)

-Aeromonas

-Scedosporium

This patient end up having multiple organisms growing: PA+SA as well as Aeromonas

4 days later her developped rapidly progressing necrotic skin lesions that showed:

-Broad aseptate hyphae!! Rhizopus–> cutaneous mucormycosis in immunocompetent due to trauma or burn! (Ecthyma like)

This reminded me of a patient that comes for necrotizing fascitis after trauma found to be due to Mucormycosis.

We had a presentation today:

Patient with AML on Levaquin, Vori prophylactically gets admitted for SCT found to have a line infection that grew yeast.

I decided to make the discussion:

Yeast forms:

• MDR Candida
• Trichosporon
• Malassezia furfur
• Cryptococcus (not usually line related)
• Rhodotorula (was the diagnosis in our case)
• Saccharomyces
• I put the other yeast forms that no one objected even they should have objected:
  • Endemic Mycoses: Histo, Cocci, Blasto: They do NOT cause line infection but also the mistake that no one told me about is: YEAST in tissue BUT grow as a MOLD!

In this case it was a Rhodotorula that has a funny sensitivity. Usually Fluco resistant.

Also a tip for the board: Rhodo: red yeast!

Also in this case, M. presented the case as Caspo resistant yeast and they added Fluconazole: it is a joke obviously, because patient has been on Voriconazole: you need to go with Amphotericin until final ID and sensitivity available.

Management: Ampho and remove the line

I had a patient with HIV who comes for SBO, end up having fever, so Cefepime was started for gram negative bacteremia and patient still spiking fevers more than ever.

The final result: Gram negative growing from the anaerobic bottle: Bacteriodes! Cefepime evidently not doing the job.

GI source of infection: do not forget anerobes.

I was consulted on a neutropenic fever and patient CT Scan showed some swelling possible cellulitis but could not find it.

Next day, I come to see the patient intubated because of respiratory failure, and the resident on call order a lactic acid!

Lactic acid was 10!! without hypotension.

So it was evident that something is dying! and we found a black skin in the inguinal area on the buttocks: necrotizing cellulitis, it could have been necrotizing fascitis and fournier gangrene. She end up requiring major skin debridement and wound Vac.

The other old trick: A normal BP is Hypotension if the patient is usually hypertensive.

Lactic acid: good test to order

Beware of Gamma-Strep : It is enterococcus until proven otherwise. That means difficult to kill, may cause IE, and may be very resistant such as VRE.