Septicemia-Is the immune response to organisms in the blood, resulting in a cytokine storm.  This, obviously can cause septic shock.

Bacteriema and viremia are simply terms denoting presence in blood.

Define: Endocarditis

Differentiate:

Acute endocarditis

Subacute endocarditis

Endocarditis: Infection of the endocardium lining the heart valves.

Acute- Displays NORMAL heart valves (unless they are prosthetic). Rapid onset; causes high fever, chills, heart murmur, fatigue, weight loss and ultimately congestive heart failure

"acute endo quickly Makes Frail Fellows Cold, Congested, and Whithered with Normal heart valves."

Subacute is usually brought up by underlying structural damage (such as a prosthetic valve), is more chronic (weeks to months), has less severe symptoms and can cause skin lesions known as Osler's nodes (look almost like a raised pin prick; often compared to stigmata).

Name the bacteria responsible for Acute Endocarditis

Name the bacteria responsible for Subacute Endocarditis

Acute: S. aureus (leading cause) or A/B streptococcus

Subacute: Staphylococcus epidermidis, Streptococcus viridans (salivarius, mutans, mitis) or Enterococcus

What is "green strep"?

What are some characteristics of this bacteria?

The alpha hemolytic appearance of streptococcus viridans.  This species is catalase negative and can be differentiated from other streptococcus strains b/c it is resistant to the antibacterial Optochin.

Streptococcus viridans are normal flora of the nasopharynx, mouth (causes dental carries) and GI tract.

S. Salivarius, S. Mutans, S, Mitis.

"Someone Save the Mutant Mice!"

Extracellular glucans/dextrans (allows dental binding).  Gingivitis can cause bacteremia of this species, leading to subaccute endocarditis.

FimA-surface adhesion; allows firbronectin binding which is the causative agent behind subacute endocarditis.

An immunocompromized patient is recently diagnosed with endocarditis, however the cultured bacteria from the patient's blood are non-hemolytic/barely alpha hemolytic.  This patient also has a persistent UTI.

What kind of bacteria probably caused this endocarditis?

Why is it important to identify which bacteria is the causative agent?

Probably caused by Enterococcus, a group D streptococci.

This bacteria often causes disease opportunistically, and is usually non-hemolytic.

Can also cause UTIs, infect wounds, and cause intra-abdominal infections.

It is important to identify because it is resistant to methicillin, and some are even resistant to vancomycin (VRE plasmid acquired).  This is a necessary consideration for treatment as opposed to a treatment for staphlococcus aureus.

What disease often precedes Rheumatic Fever?

What strain of bacteria often causes this preceding disease?

What are the key virulence factors of S. Pyogenes in:

Endocarditis

Rheumatic Fever

Toxic Shock Syndrome

Endocarditis:

Capsule-resistance to complement

M Protein-resistance to complement, adherence

Protein F-binds fibronectin

Protein G-binds Fc portion of antibodies.

Rheumatic Fever

M protein- causes antibody cross reactivity, thus inducing autoimmune disease of the heart in rheumatic fever.

Toxic Shock syndrome

SPE-A: A very potent super antigen which can cause shock, and possibly death.

Autoimmune type 2 hypersensitivity reaction

Antibodies directed against M-protein cross-react with heart myosin

Damages heart valves

Those recovering require prophylactic antibiotics when undergoing dental procedures

Prevention is in treating pharyngitis within 9 days of onset for best preventative results.

Staphylococcus aureus (Toxin TSST-1 superantigen) Bacteremia is RARE!

Streptocccus pyogenes (Technically called Toxic Shock Like Syndrome caused by the toxin superantigen SPE-A)  High mortality.  Can see bacteremia.

rapid Fever

Vomiting

diarrhea

Diffuse erythematous rash

Hypotension

Desquamation during recovery

Mechanical-no development of parasite in vector

Biological-some stages of life cycle in vector

What protozoan genus is the causative agent of Malaria?

What species?

Plasmodium

Species:

Vivax (80%) reticulocyte preference

Falciparum (15% but very deadly) can infect all RBC ages

Malariae (minimal) older RBCs

Ovale (minimal) reticulocyte preference

Only Vivax and Ovale can cause malaria relapse.

– Chloroquine – resistance common

– Quinine + doxycycline (for resistant strains)

– Primaquine – also effective against dormant parasites

A patient enters your office with a high acute fever, malaise and cold sweats.  The patient reports no travel to other countries, let alone the state of NJ, for the past 10 years.  What might be a likely diagnosis?

What are some key characteristics of this disease?

Babesiosis

1-4 week incubation period, gradual onset

presents as a "summer flu" with fever, chills, sweating etc.  Can also cause splenomegaly as RBCs are destroyed by the parasite.  NOTE: No liver stage like that seen in Malaria.

Often transferred by the deer tick, a.k.a Babesia microti which is the definitive host.

A female patient enters your office with flu-like symptoms that are self limiting. These symptoms have been present for a much longer time than an average flu, and allergies (as attended to by an allergist) are not an issue.

As a side note, this patient is also actively attempting to become pregnant. 

What would you suggest as a differential diagnosis?

Toxoplasmosis caused by Toxoplasma gondii is one possible candidate.  A bronchoalveolar lavage with crescent shaped trophozoites is diagnostic.

This disease can have severe CNS consequences or even fatality/reoccurance in immunocompromized patients.

Also, Congenital infections can be very severe.

Cats; can be transmitted to humans through raw meat as tissue cysts, cat feces or congenitally.

1. Ingest oocysts

2. Enter macrophages

3. Asexual reproduction occurs in macrophages

4. Rupture and release of new parasites -trophozoites

5. Invade any nucleated cell (MHC-I; Parasites destroyed) Brain, heart, skeletal muscle - formation of tissue cysts

Wuchereria bancrofti (a nemotode with a mosquito vector).

These organisms exhibit circadian periodicity:

pulmonary vessels - day

peripheral circulation - night

Infection causes inflammatory damage, fever, lymphadenitis, lymphatic obstruction.  Repeated infections can lead to elephantiasis.

Humans are actually the definitive host!

Infection by Schistosoma japonicum, mansoni or haematobium via their presence in fresh water through snails as an intermediate host.  Humans are the definitive host.

Japonicum and mansoni release eggs in feces, while haematobium releases eggs in urine.

Clinical symptoms -

– Early - (migration of larvae) - fever, cough, abdominal pain,

hepatosplenomegaly, eosinophilia

– Late - (response to eggs) adults may live 3-8 yrs

- granulomas, fibrosis (damage) of organs (hepatic, renal,

intestinal)