P LANIFICACIÓN DEL LEVANTAMIENTO DE REQUISITOS

The pathophysiologic consequences and clinical manifestations of infective endocarditis can be explained by the following:

1. Cytokine production, which is responsible for constitutional symptoms (ie fever) 2. Embolization of vegetation fragments, which lead to infection or infarction of remote tissues.

3. Hematogenous spread of infection during bacterium.

4. Tissue injury from immune complex deposition or immune response to deposited bacterial antigens.

Subacute infective endocarditis: Remember that patients can have sub acute infective endocarditic secondary to dental surgery. Viridans group streptococci are the most likely cause of endocarditis in native valves following dental procedures. 4 members of the viridans group cause it: strep. Mitis, s. sanguis, s. mutans, and s.

salivarius. S. mutans also causes dental carries.

Staph. Aureus is the major cause in IV drug abusers, but causes ACUTE infective endocarditis.

Staph. Epidermidis is the m.c cause of infective endocarditic in pts with prosthetic valves.

Staph. Saprophyticus usually causes UTI in young women.

Strep. Bovis endocarditis is associated with colon cancer.

Enterococcus is less frequent, but is seen in lower GU procedures and causes endocarditis.

IV drug abusers with fever and new onset murmurs have acute infective endocarditic.

The m.c cause is staph. Tx with vancomycin + gentamicin because it covers staph, strep, and enterococci. Furthermore, beta lactam antibiotics are synergistic with amino

glycosides.

If the pt is not a drug user, then nafcillin OR cefazolin AND gentamicin.

In cases of suspected infective endocarditis, blood cultures should be obtained immediately and empiric antibiotic therapy should be started afterwards.

Remember that some pts have pulmonary infection in the setting of IV drug abuse.

This is highly suggestive of septic embolism from infective endocarditis involving the tricuspid valve, esp if x-ray shows cavitating lung nodules.( Had 3 CT pix)

Currently the m.c predisposing factor to native valve endocarditis in the US is mitral valve prolapse. Previously rheumatic valvular damage was the leading cause of native valve endocarditic, but this is no longer the case. The mitral valve is the m.c

affected valve in pts who are NOT drug abusers, and mitral regurgitation is the m.c valvular abnormality observed in these pts.

Roth spots are exudative, edematous lesions on the retina. They appear as oval hemorrhages, with pale centers. The underlying cause is an immune vasculitis. They are an infrequent finding in pts with IE. They have also been noted in pts with collagen vascular disease and hematologic disorders, such as severe anemia.

Immune activation is also thought to be responsible for osler’s nodes, IE-associated glomerulonephritis, and the rheumatologic manifestations of IE osler’s nodes are violaceous nodules on the pulp of the fingers and toes thought to be caused by immune complex deposition.

Strep. Bovis endocarditis is associated with colorectal cancer. Colonoscopy should be pursued for further evaluation. Not stool guaiac testing.

IE duke criteria : -Blood culture - TEE

Order: bld culture IV empirics TEE TTE tricuspid endocarditis

If not IV drug user genta+ nafcillin/cefazolin

s. epidermidis also seen in infants with IE sec to umbilical venous catheter infection in neonatal intensive care units.

HIV:

In an HIV infected patient, if you see a bright, red, firm, friable, exophytic nodule, its most likely bacillary angiomatosis. To tx it give oral erythromycin.

PCP can cause nodular and papular cutaneous lesions of the external auditory meatus.

Polyvalentpneumococcal vaccine is recommended in all children and adults with HIV infection and a CD4 count above 200 cells/microL.

Hepatitis A vaccine is recommended for HIV infected patients who are suffering from hepatitis b, C, or both. It is also recommended for IV drug users and in patients with preexisting liver disease.

Meningitis vaccine is SUBOPTIMAL in HIV patients, but it is recommended for any patient with a appendectomy or functional asplenia, or for pts traveling to high risk countries.

Acute HIV may present with an influenza-like syndrome consisting of fever, fatigue, diffuse lymphadenopathy, nausea, vomiting, and a maculopapular rash classically

involving ulceration of the oropharynx. D/D Mono

If you suspect toxoplasmosis in an AIDS pt, tx with pyrimethamine and sulfadiazine.

On CT you see multiple ring enhancing lesions. If lesions to not respond to tx, then do brain biopsy.

Brain irradiation is used in the management of primary CNS lymphoma. Lesions are weakly enhancing and usually single.

All pts who are diagnosed with HIV infection should receive the following:

1. H & P.

2. Chemistry and hematology.

3. 2 plasma HIV RNA levels.

4. CD4 T cell count.

5. VDRL test.

6. PPD.

7. Anti-toxoplasma antibody titer.

8. Mini mental status exam.

9. Pneumococcal vaccine, unless CD4 count is less than 200.

10. Hep A and B serology.

11. Hep A and B vaccine, if seonegative.

12. HHIV counseling.

13. Info and assistance for those who might have been infected by the subject.

The lesions of Kaposi sarcoma are cutaneous, asymptomatic, elliptical, and arranged linearly. They involve usually the legs, face, oral cavity, and genitalia. The lesions begin as papules, and later develop into plaques or nodules. The color typically changes from light brown to violet. There is no associated necrosis of the skin or underlying structures.

It is m. c seen in homosexual HIV pts and caused by human herpes virus 8.

Pneumonia in HIV:Suspect bacterial pneumonia in an HIV infected patient who presents with acute onset, high grade fever and pleural effusion. Pneumococcus is the most common cause of pneumonia in HIV pts. Due to their impaired humoral immunity, HIV patients are susceptible to infection by encapsulated organisms in general, so other encapsulated bacteria should also be considered in the differential.

Esophagitis occurs with advanced HIV disease, usually when the CD4 count is less than 50/microL. The typical presentation is when the HIV infected patient complains of painful swallowing and substantial burning.

1- Candida The m.c etiologic agent of esophagitis in HIV infected patients is candida; therefore such patients are first started on fluconazole. Failure to respond to a 3-5 day course of oral fluconazole warrants further investigation.

The next step is to perform esophagoscopy with cytology, biopsy, and culture to determine the specific etiology. Examples of other causative agents are HSV and CMV.

2- CMVHIV patients with severe odynophagia but without oral thrush are likely to have ulcerative esophagitis, which is most often caused by CMV. The triad of :

• 1.Focal substantial burning pain with odynophagia,

• 2. Evidence of large, shallow, superficial ulcerations, and

• 3. Presence of intramuscular and intracytoplasmic inclusions is diagnostic of CMV esophagi is. The t of choice is IV acyclovir.

3- Herpes simplex esophagitis also a common cause of esophagi is in HIV patients. These ulcers are usually multiple, small, and well circumscribed and have a “volcano-like” (small and deep) appearance. Cells show ballooning degeneration and eosinophilic intramuscular inclusions.

Fluconazole is used for prophylaxis against Cryptococcus and coccidioides in HIV positive pts who have had these diseases in the past.

Cyrstal-induced nephropathy is a well-known side efx of Indinavir therapy

(protease inhibitor). It is caused by precipitation of the drug in the urine and obstruction of the urine flow. For many reasons, some clinicians recommend periodic monitoring of U/A and serum creatinine levels every 3 to 4 months.

Remember the following common acute life-threatening reactions associated with HIV therapy:

• Didanosine: pancreatitis.

• ^Hypersensitivity

• Lactic acidosis: use of any NRTI’s

• Steven Johnson syndrome: use of any NNRTI

• Nevirapine: liver failure.

Remember that if the pts CD4 count is less than 50, they may have an atypical mycobacterium infection, esp in light of the fact that the pt has no past history of or exposure to tuberculosis.

The differential includes MAI, TB, disseminated CMV, and non-hodgkins lymphoma. All HIV infected pts with a CD4 count < 50/mm3 should receive azithromycin as prophylaxis against MAI

Diarrhea in HIV : In HIV infected patients, diarrhea can be due to a variety of organisms. To identify the causal organism prior to instating therapy, do a stool culture, exam the stool for ova and parasites, and test for c. dificile toxin.

HIV pts with CD4 cell counts less than 50/miroL require prophylaxis against MAI with azithromycin or clarithromycin. Rifabutin is used as an alternative to macrolides for MAI prophylaxis.

Pts with CD4 counts less than 100 and live in areas endemic for histoplasmosis require prophylaxis with itraconazole.

Oral acyclovir may be effective for prophylaxis against CMV infection.

Valacyclovir is the drug of choice for the tx of herpes zoster; acyclovir is an alternate.

post herpetic neuralgia can be prevented and/or treated with TCA’s.

In an HIV infected patient, bloody diarrhea and a normal stool exam are highly suspicious for CMV colitis and warrant a colonoscopy with biopsy. CMV is a common opportunistic pathogen in HIV infected pts and may cause esophagitis, colitis, proctitis, gastritis, and small bowel disease. Pts with CMV colitis present with chronic bloody diarrhea, abdominal pain, and a CD4 count less than 50 cells/uL. Colonoscopy shows multiple mucosal erosions and colonic ulceration. Biopsy shows the presence of large cells with eosinophilic intranuclear and basophilic intracytoplasmic inclusions (“owl’s eye” effect). Tx with acyclovir, or foscarnet.

Vs. cryptosporidiosis: causes profuse, watery diarrhea. NO blood or giant cells on colon biopsy.

Vs. E. histolytica: is a parasite that causes bloody diarrhea. On stool exam you can see trophozoites. Colonoscopy shows the presence of flask-shaped colonic ulcers.

MAI: disseminated infection can cause chronic diarrhea and weight loss; however, the diarrhea is NON bloody and generally involves the small intestine. Do a biopsy with culture to dx.

PCP: the drug of choice is tmp-smx. When it is not available or contraindicated, the alternative is a 14 day course of IV/IM pentamidine. It has a number of side efx

including hypoglycemia, hyperglycemia, hypocalcaemia, azotemia, or liver dysfunction, pancreatitis.

In the HIV patients, if they have a bilateral interstitial opacification without hilar lymphadenopathy, cavitation, pleural effusion, or cardiomegaly, this would also be consistent with atypical pneumonia secondary to an organism such as mycoplasma or Chlamydia. Thus, azithromycin should also be given until testing confirms PCP.

Remember that PCP is an AIDS-defining illness.

Antiretroviral therapy:

Before strating therapy

• Hx,Px

• CBC, bld chemistry, serum transminases and lipid profile

• CD4 count

• Plasma HIV RNA titer

Post exposure prophylaxis Do serology and start 3 drugs. Repeat testing at 1.5 , 3 and 6 months.