Tag Archives: Infectious Disease

Answer to CC #17

Case challenge #17 presented an 85-year-old Caucasian male with “bony protrusions” on his gums and the following histologic findings:

Casechallenge 17

Which of the following is the best initial treatment?

CC17 Voting

The correct answer is: IV Penicillin G

The image above reveals infection by a the filamentous, gram-positive, non-acid fast, anaerobic bacteria, ACTINOMYCES.

Background

  • Subacute-to-chronic bacterial infection caused by filamentous gram positive, non-acid fast, anaerobic bacteria
  • Most common clinical forms of actinomycosis are cervicofacial, thoracic, and abdominal
  • Endemic world-wide
  • Thoracic actinomycosis accounts for 15-20% of cases. Aspiration of oropharyngeal secretions containing actinomycetes is the usual mechanism of infection.

Clinical Presentation

  • Cervicofacial, thoracic, abdominal, and CNS infections:
  • Often present with: dry or productive cough, blood streaked sputum, shortness of breath, fevers, weight loss, fatigue, anorexia

Diagnosis

  • Direct identification and/or isolation of the organism from a clinical specimen
  • Sulfur granules

Management

  • Preferred regimen: Pen G IV for 2-6 weeks, then amoxicillin PO for 6-12 months
  • Doxycycline, minocycline, tetracycline, clindamycin, erythromycin, and cephalosporins have been proven to be effective in case reports

Case Challenge 18, next week!

Internal Medicine Journal Watch – April 2015

STRAIGHT FROM THE HOUSESTAFF – the April 2015 UT Southwestern Internal Medicine Journal Watch! They have summarized important issues in clinical practice, from alcoholic hepatitis to which medications to use for stroke prevention in afib. Make sure to take the EKG challenge at the end! You will have to view this post on our website to access the PDF.  There is a quick run down of the topics below:

Hepatology

  • Corticosteroids in severe alcoholic hepatitis after recent upper GI bleed. Dr. Jan Petrasek reviewing Rudler et al., J Hepatol. 2015 Apr;62(4):816-21. 10.1016/j.jhep.2014.11.003. Epub 2014 Nov 11.
  • Serum ammonia level for the evaluation of hepatic encephalopathy. Dr. Jan Petrasek reviewing Ge et al., JAMA. 2014 Aug 13;312(6):643-4.

Rheumatology

  • Extended report: Prediction of cardiovascular risk in rheumatoid arthritis: performance of original and adapted SCORE algorithms. Dr. Brian Skaug reviewing Arts, et al. Ann Rheum Dis. 2015 Feb 17. pii: annrheumdis-2014-206879. doi: 10.1136/annrheumdis-2014-206879

Pulmonary/Critical Care

  • Trial of Early, Goal-Directed Resuscitation for Septic Shock [The Protocolised Management in Sepsis (ProMISe) Trial]. Dr. James Galloway reviewing Mouncey PR et al. N Engl J Med. 2015;372(14):1301-11.
  • A Randomized Trial of Icatibant in ACE-Inhibitor-Induced Angioedema. Dr. James Galloway reviewing Bas M, et al. N Engl J Med. 2015;372(5):418-25.

Nephrology

  • High-Sensitivity Troponin T and N-Terminal Pro-B-Type Natriuretic Peptide (NT-proBNP) and Risk of Incident Heart Failure in Patients with CKD: The Chronic Renal Insufficiency Cohort (CRIC) Study. Dr. Natalia Rocha reviewing Bansal N, et al. JASN 2015; 26:946-956
  • Preoperative renin–angiotensin system inhibitors use linked to reduced acute kidney injury: a systematic review and meta-analysis. Dr. Natalia Rocha reviewing Cheungpasitporn W, et al. Nephrol. Dial. Transplant. 2015; doi: 10.1093/ndt/gfv023

Cardiology

  • Which drug should we use for stroke prevention in atrial fibrillation? Dr. Douglas Darden reviewing Lau, Yee C.; Lip, Gregory Y.H. Current Opinion in Cardiology. 2014 July 29 (4): 293-300.
  • EKG CHALLENGE: Contributed by Dr. Jeanney Lew

Screen Shot 2015-04-29 at 10.49.07 PM

All of the work above comes from the IMJW Editorial Board: Jan Petrasek, Brian Skaug, Ben Galloway, Natalia Rocha, Doug Darden, and Jeanney Lew!

Disseminated Histoplasmosis

  • Basic Information

    • AIDS defining illness and typically seen in HIV patients with CD4<100 cells/microL.
    • The fungus (Histoplasma capsulatum) is found in soil contaminated with bird or bat excreta and transmission occurs from inhalation of spores.
    • Thought to be endemic in Ohio, Mississippi, Caribbean, Mexico, Asia, and Central/South America.
  • Clinical Manifestations

    • Immunocompromised hosts can present with more severe symptoms: fevers, night sweats, nausea, vomiting, dyspnea.
    • 50% of AIDS patients with disseminated histoplasmosis have pulmonary involvement.
  • Diagnosis

    • Elevated LFT’s, LDH, and ferritin are commonly seen. Elevated creatinine is considered a poor prognostic factor.
    • Although the initial chest x-ray often looks normal, may see diffuse interstitialor reticulonodular infiltrates.
    • Most sensitive and specific test for suspected disseminated histoplasmosis in an HIV patient is histoplasmosis antigen detection.
    • Histoplasmosis antigen can be detected in fluids including urine, serum, cerebrospinal fluid.
  • Management

    • Rapid initiation of treatment is important and includes induction and maintenance phases. Amphotericin B is typically used for induction for 1-2 weeks. Therapy is then switched to itraconazole for consolidation and long-term suppression.
    • 2009 IDSA guidelines recommend primary prophylaxis with itraconazole for HIV patients with CD4<150.

Food-borne Botulism

(The previous, incomplete entry was posted in error – here is the revised, complete version)

In the news this week, we have another food-borne outbreak, botulism in Ohio. Following up on our post about listeria, lets see what botulism has in store (no pun intended).

Introduction

Foodborne botulism is caused by ingestion of foods contaminated with botulinum toxin, causing a distinct clinical syndrome of symmetrical cranial nerve palsies followed by descending, symmetric flaccid paralysis of voluntary muscles, which may progress to respiratory compromise and death. The mainstays of therapy are meticulous intensive care (including mechanical ventilation, when necessary) and timely treatment with antitoxin.

The Organism and its Toxins

  • Organism
    • Clostridium botulinum is ubiquitously found in soil and aquatic sediments.
    • C. botulinum grows and elaborates toxin only when the food presents conditions that include an anaerobic milieu, a pH of 4.5, low salt and sugar content, and a temperature of 4C–121C.
  • Toxin
    • Human cases are caused mostly by toxin types A, B, E, and (rarely) F.
    • The toxins exert their action on the cholinergic system at the presynaptic motor-neuron terminal by blocking acetylcholine transmission across the neuromuscular junction, causing neuromuscular blockade, resulting in flaccid paralysis. The toxins also affect the adrenergic system, but this apparently happens without significant consequences.
    • In contrast with the spore, botulinum toxins are temperature sensitive, and all toxins are inactivated by heating to 85C for 5 min.
  • Spores
    • Under stress, C. botulinum forms a spore that survives standard cooking and food-processing measures.
    • The technique of modern industrial canning (i.e., retort canning) was developed expressly for killing C. botulinum spores.
    • Spores do not germinate in the human intestine – ingestion of spores is not toxic

Clinical Manifestations

  • Cranial nerve palsies are invariably presenting symptoms of botulism. The absence cranial nerve palsies or their onset after other true neurological symptoms have made their appearance rules out the disease.
  • Gastrointestinal symptoms (nausea and vomiting) may precede neurological symptoms
  • Flaccid, descending, completely symmetric paralysis of voluntary muscles, affecting (in order) the muscles of the neck, shoulders, the proximal and then distal upper extremities, and the proximal followed by distal lower extremities.
    • Paralysis of the diaphragm and accessory breathing muscles may result in respiratory compromise or arrest
    • Constipation is a nearly universal symptom
    • Deep tendon reflexes progressively disappear
  • Rate of progression and severity are proportional to the dose of toxin
  • The sensory system is unaffected. Intellectual function is preserved throughout.
  • Death in patients with untreated botulism results from airway obstruction from pharyngeal muscle paralysis and inadequate tidal volume, resulting from paralysis of diaphragmatic and accessory respiratory muscles.

Differential Diagnosis

  • GBS, myasthenia gravis, stroke syndromes, Eaton-Lambert syndrome, and tick paralysis.
  • Less likely conditions include tetrodotoxin and shellfish poisoning, antimicrobial-associated paralysis, and a host of conditions due to even rarer poisons.

Diagnosis

  • Routine laboratory tests and radiological studies are not useful for diagnosis of botulism.
    • Lumbar puncture reveals normal CSF values—in particular, the protein level is normal, in contrast to Guillain-Barre´ syndrome (GBS).
    • Brain imaging studies may help rule out rare stroke syndromes that produce nonlateralizing symptoms.
    • The Tensilon test helps for diagnosis of myasthenia gravis.
    • EMG: can be an exceedingly helpful adjunct to diagnosis. In affected muscles, findings consistent with neuromuscular junction blockage, normal axonal conduction, and potentiation with rapid repetitive stimulation are indicative of botulism
  • Specialized testing: only performed in a few labs around the country
    • Confirmation of botulism rests on demonstration of the toxin in specimens of patient serum, gastric secretions, or stool or in a food sample
    • Demonstration of C. botulinum in a patient’s stool sample or in cultures of wound material is generally satisfactory for diagnosis of adult botulism syndromes

Management

  • Management with supportive intensive care and anti-toxin must begin before diagnosis is confirmed, as specialized testing can take up to 48 hours at reference labs (plus transit time for the specimen).
  • Call the state health department immediately to speak to an expert!
  • Supportive intensive care
    • Frequent monitoring of vital capacity and institution of mechanical ventilation if required.
    • Paralysis due to botulism is protracted, lasting weeks to months, and meticulous intensive care is required during this period of debilitation.
  • Anti-toxin
    • Can arrest the progression of paralysis and decrease the duration of paralysis and dependence on mechanical ventilation
    • Should be given early in the course of illness, ideally <24 h after onset of symptoms, because antitoxin neutralizes only toxin molecules that are yet unbound to nerve endings.
    • Adverse effects: anaphylaxis, other hypersensitivity reactions, and serum sickness
    • Before administration of antitoxin, skin testing should be performed to test for sensitivity to serum or antitoxin.

Modified from Clinical Infectious Diseases 2005; 41:1167–73

Cryptococcal Meningitis- Thinking Beyond HIV

This week at morning report we talked about cryptococcal meningitis with Dr. James Luby from UTSW ID Division. Typically associated with HIV, Dr. Luby told us that there are conditions that can be associated with this infection such as liver disease like cirrhosis, end stage renal disease, and diabetes. A study was published in 2011 in Yonsei Medical Journal which was a retrospective look at patients with and without HIV who had diagnosed cryptococcal meningitis. Their findings included:

  • 20 total patients included in the study, 11 of which had HIV
  • Single center study at Pusan National University College of Medicine in South Korea
  • Other conditions were diabetes, end stage renal disease, and liver disease
  • There was no significant difference in mortality between HIV and non-HIV patients
  • No statistically significant differences in serum CRP level and other cerebrospinal fluid parameters between patients with HIV and without HIV

Below is some basic management points for cryptococcal meningitis courtesy of The Hopkins ABX Guide:

  • Diagnosis: positive fungal culture or cryptococcal antigen in CSF
  • CSF cryptococcal Ag positive >95% (serum-100%), India ink positive stain in CSF – 75%, CSF fungal culture>95%
  • Typical CSF profile: protein 30-150mg/dL, monocytes 0-100, Opening pressure>200mmH2) in 75% of cases
  • Treatment
    • Induction Phase: Amphotericin B + flucytosine >14 days and then fluconazole
    • Maintenance Regimen: Fluconazole 200mg/daily PO indefinitely unless CD4>200 for 3 months or 12 months minimum in non-HIV patients and asymptomatic
    • If opening pressure >250mmH2), CSF drainage until <200mmH2O or >50% reduction, repeat daily until OP stable
    • Consider LP or VP shunt if elevated pressures persist

Check out the study below and the IDSA guidelines for management of cryptococcal disease:

Cryptococcal meningitis in patients with or without human immunodeficiency virus: experience in a tertiary hospital

2010 IDSA Guidelines for Management of Cryptococcal Disease

(Image courtesy of Jennifer Lodge)