Urinary tract infections are a common problem seen in both the outpatient and inpatient setting. For community-acquired UTIs, (KEEPS) is a helpful mnemonic to remember the common pathogens:

Klebsiella (~10%)

E. coli (~80%)


Proteus mirabilis (5%)

S. saphrophyticus (5-10%) 

NOTE: in the hospital, remember to consider: Pseudomonas, Serratia and Staph aureus!!!

Campylobacter jejuni has been shown by several studies to be strongly associated with Guillain-Barré syndrome (GBS). In the landmark Kuroki et al. study C. jejuni was found in approximately 30% of GBS patients compared with only 1.2% of a healthy control population. Several studies have demonstrated similar findings. Another notable cause is cytomegalovirus (CMV).


  1. Kuroki S, Saida T, Nukina M, Haruta T, Yoshioka M, Kobayashi Y, Nakanishi H. Campylobacter jejuni strains from patients with Guillain-Barre syndrome belong mostly to Penner serogroup 19 and contain B-N-acetylglucosamine residues. Ann Neurol. 1993;33:243–247.
  2. Nachamkin I, Allos BM, Ho T. Campylobacter Species and Guillain-Barré Syndrome. Clinical Microbiology Reviews. 1998;11(3):555-567.

Splenectomy may be necessary 2° to: 1) trauma 2) cancer (i.e multiple myeloma, ALL, CLL) 3) ITP refractory to treatment. Certain disease states may result in functional asplenia (i.e Sickle cell disease).

REMEMBER *SHIN* for encapsulated organisms:

Streptococcus pneumoniae

Haemophilus Influenzae

Neisseria meningitidis

NOTE: The risk of sepsis after splenectomy is highest in the first couple of years!


  1. Capnocytophaga canimorsus – Increased risk from cat and dog bites
  2. Babesia microti- Tick precautions when at risk for tick exposure in areas of risk 
  3. Salmonella typhi- Leading cause of Osteomyelitis in Sickle Cell patients


  1. Principles and Practice of Hospital Medicine.  Chapter 198. Infections of the Immunocompromised Host. Sarah P. Hammond, MD; Lindsey R. Baden, MD
  2. 374: Primary Immune Deficiency Diseases. Harrison’s Principles of Internal Medicine, 19. Alain Fischer

Definition: a temperature >38.3 C (101 F) for at least three weeks’ duration AND failure to identify a source after one week of appropriate medical workup.


  1. Approach to the Adult Patient with Fever of Unknown Origin. ALAN R. ROTH, D.O., and GINA M. BASELLO, D.O., Jamaica Hospital Medical Center, Mount Sinai School of Medicine Family Practice Residency Program, Jamaica, New York. Am Fam Physician. 2003 Dec 1;68(11):2223-2229.

Both are first generation penicillins

Pencillin G => IV or IM

Penicillin V (phenoxymethylpenicillin) => more acidic, more stable and can be given orally (PO). Penicillin VK is just its potassium salt.

NOTE: Penicllin V is less active against gram-negative bacteria then than penicillin G .


Nathwani D, Wood MJ. Penicillins. A current review of their clinical pharmacology and therapeutic use. Drugs 1993;45:866-94.

Mycobacterium tuberculosis is an obligate aerobe and only survives in oxygenated areas.tb-upper-lobe

Exact reason for TB’s propensity to reactivate in the upper lobes is not clear but two proposed rationales:

  1. Relatively higher oxygen tension compared to lower lobes (The lower lobes have better perfusion and therefore better V/Q match => greater gas exchange and more CO2 content compared to upper lobes)
  2. Impaired lymphatic drainage in upper lung lobes reduces the ability of the immune system to mount a response to the pathogen and clear it


  1. Allen EA. Tuberculosis and other mycobacterial infections of the lung. In: Thurlbeck WM, Churlbeck AM, eds. Pathology of the lung. 2nd ed. New York, NY: Thieme Medical, 1995; 229-265.
  2. Goodwin RA, DesPrez RM. Apical localization of pulmonary tuberculosis, chronic pulmonary histoplasmosis, and progressive massive fibrosis of the lung. Chest 1983; 83:801-80
  3. Dolin, [edited by] Gerald L. Mandell, John E. Bennett, Raphael (2010). Mandell, Douglas, and Bennett’s principles and practice of infectious diseases (7th ed.). Philadelphia, PA: Churchill Livingstone/Elsevier. pp. Chapter 250.

Why give Clindamycin for a Group A Strep infection that is already adequately covered by a Beta-lactam?

Proposed rationale: Clindamycin blocks 50s ribosomal subunit and therefore inhibits bacterial protein synthesis. It is thought that this will reduce endo/exotoxin production which is how Streptococcus pyogenes elicits its pathogenic effect. (It also increases opsonization and phagocytosis by inhibiting M-protein synthesis). Hence, it will act synergistically with the Beta-lactam (which is destroying the cell wall) to reduce the amount of toxin that is subsequently released into the blood. Clindamycin has a longer postantibiotic effect than penicillin.

The exotoxins of group A streptococci include the erythrogenic toxins (pyrogenic exotoxins) and the cytolytic toxins (streptolysins S and O)


1. Stevens DL. Streptococcal Toxic-Shock Syndrome: Spectrum of Disease, Pathogenesis, and New Concepts in Treatment. Emerg Infect Dis. 1995, Sept. Available from http://wwwnc.cdc.gov/eid/article/1/3/95-0301

 2. Marek, S. Current indications for the use of clindamycin: A critical review. Can J Infect Dis. 1998 Jan-Feb; 9(1): 22–28. 

3. Kalyan S, Chow AW. Staphylococcal toxic shock syndrome toxin-1 induces the translocation and secretion of high mobility group-1 protein from both activated T cells and monocytes. Mediators Inflamm. 2008. 2008:512196.

Why is oral (PO) Vancomycin given for C. Difficile? Why not IV?

MECHANISM: Vancomycin is a large, hydrophilic molecule that for the most part is not absorbed across the gastrointestinal mucosa (it has low bioavailability). Hence when given PO, it will accumulate in the GI tract and reach sufficient concentrations for therapeutic effect. 


1. Van Bambeke F (August 2006). “Glycopeptides and glycodepsipeptides in clinical development: a comparative review of their antibacterial spectrum, pharmacokinetics and clinical efficacy”. Current Opinion in Investigational Drugs 7 (8): 740–9.

2. Edlund C, Barkholt L, Olsson-Liljequist B, Nord CE (September 1997). “Effect of vancomycin on intestinal flora of patients who previously received antimicrobial therapy”. Clinical Infectious Diseases 25 (3): 729–32.