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Infectious Disease
N. D. Agrawal, MD
Classification of Bacteria
Gram Positive Cocci
A: Staphylococcus: Arranged in grape like irregular clusters
 Coagulase Positive- Staph. Aureus
 Coagulase Negative- 1. Staph. Epidermidis (present on normal flora of skin, mostly causes infection of
prosthetic devices or infection after surgery)
2. Staph. Saprophyticus: Causes UTI
B: Streptococci: Forms pairs or chains
1: Beta hemolyticus streptococci: Produces hemolysis
 Group A- S. Pyrogens – Causes Rheumatic Fever, Erysipelas, Sore throat, Impetigo, Endocarditis,
Glomerulonephritis
 Group B- S. agalactiae- Normal flora of female genital tract causes neonatal sepsis and meningitis
 Group D- Enterococci, (S. fecalis, S.faecium) Normal flora of GI tract causes UTI, meningitis,
endocarditis
Non-enterococci: (S. Bovis) Normal flora of GI tract can cause endocarditis. If there is
bacteremia- rule out Carcinoma colon by colonoscopy.
2: Non Beta hemolytic Streptococci:
 S. Pneumoniae (Pneumococci) Causes Pneumonia, meningitis, endocarditis
 Viridans Streptococci (S. mitis, S. mutans, S. sanguis, S. salivarius)- most common cause of sub acute
endocarditis
Gram Negative Cocci
 Neisseria gonorrhoeae
 Neisseria meningitidis
Gram Positive Bacilli
A. Bacillus species
1: Bacillus Cereus- causes food poisoning
2: Bacillus anthracis – causes anthrax
B. Clostridium species
1: Clostridium botulinum causes botulism
2: Clostridium Tetani- causes tetanus
3: Clostridium Perfringens- causes gas gangrene (myonecrosis) and food poisoning.
4: Clostridium difficile- causes pseudomembranous colitis
C. Corynebacterium Diphtheriae- causes diphtheria
D. Listeria monocytogenes- causes meningitis in neonates and elderly
Gram Negative Rods
A: Enterobacteriaceae
1: Escherichia:
 Enterotoxigenic E.coli- causes travelers diarrhea
 Enterohemorrhagic E.coli causes hemolytic uremic syndrome or severe hemorrhagic colitis
2: Shigella: Gastroenteritis
3: Salmonella- Enteric fever (Typhoid), Enterocolitis
4: Klebsiella-Pneumonia, UTI
5: Proteus- Proteus and Morganella morganii are urease positive, split urea and produce ammonia, results in
alkaline urine promoting stone formation
6: Enterobacter: UTI, Sepsis
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Infectious Disease
N. D. Agrawal, MD
7: Serratia: Mostly affects hospitalized patients
B: Pseudomonas aeruginosa-
a: Wound produces blue green pus
b: Mild Otitis externa in swimmers
c: Malignant Otitis externa in diabetics
d: Ecthyma gangrenosum- hemorrhagic necrosis in neutropenic patients- necrotic center, hemorrhagic border
C: Acinetobactor Calcoaceticus- Nosocomial pneumonia
D: Moraxella: Normal flora of upper respiratory tract
E: Vibrio
a: Vibrio Cholerae
b: Vibrio parahemolyticus – diarrhea after sea food
F: Campylobactor jejuni- most common cause of bacterial diarrhea
G: Yersinia
a: Yersinia pestis- Plague
b: Yersinia enterocolitica- diarrhea
H: Francisella tularensis- Tularemia
I: Pasteurella: Bites from Cats and Dogs causing human wound.

Pleomorphic Gram Negative Rod


 Hemophilus influenza type b- sinusitis, meningitis, pneumonia
 Hemophilus ducreyi- Chancroid
 Bordetella Pertussis: Pertussis
 Brucella species

Anerobic Bacteria
1: Gram negative bacilli
Bacteroids- Bacillus fragilis

2: Gram positive bacilli


 Actinomycetes
 Nocardia
 Lactobacillus
Unusual Pathogen
 Legionella Pneumophila- small aerobic gram negative bacteria
 Chlamydia- small gram negative bacteria
 Spirochete-Flexible helical rods. Treponema pallidum, Borrelia burgdorferi, Leptospirae
 Rickettsiae
Antibacterial Agents
 Beta Lactum antimicrobial- Penicillin, Cephalosporin, Carbapenem, Monobactum.
Penicillin:Mostly covers gram +ve, some gram –ve. It interferes with bacterial cell wall synthesis. It
inactivates the proteins involved in cell wall synthesis and inhibits transpeptidase which forms cross-linkage
between peptidoglycans.
 Penicillinase Resistant Penicillin- DOC for Staphylococcal infection- Methicillin, Oxacillin, Nafcillin,
Cloxacillin, Dicloxacillin. Some bacteria produce penicillinase, which is a beta-lactamase. It can
hydrolyze the beta-lactam ring of penicillin and make it ineffective.

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Infectious Disease
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 Extended spectrum penicillin: They have better coverage of gram negative bacilli besides gram positive.
Ampicillin, Amoxicillin (Less diarrhea than ampicillin).

 Antipseudomonal Penicillin- Piperacillin, Azlocillin, Mezlocillin, Ticarcillin


 Combination of Penicillin and Beta Lactamase inhibitor- Clavulinic Acid, Sulbactum, Tazobactum
Amoxicillin + Clavulinic Acid- Augmentin (Oral)
Ampicillin + Sulbactum- Unasyn (IV)
Ticarcillin + Clavulinic acid- Timentin
Piperacillin + Tazobactum- Zosyn
Better coverage including anerobes.

Cephalosporins: Mechanism of action is same like penicillin, inhibit bacterial cell wall synthesis. They are
highly resistant to penicilliniase. It has cross reactivity with penicillin allergic patients.
 First generation-Cefazolin, Cephalexin (Oral), Cephalothin, Cephapirin, Cephradine
 Second generation-Cefoxitin, Cefuroxime, Cefuroxime axetil (Oral), cefotetan, cefaclor, cefamandole
 Third generation-Ceftriaxone, Cefotaxime, Ceftazidime, Cefixime (Oral), Cefoperazone
 Fourth generation-Cefepime
 Fifth generation-Ceftaroline
 Second and third generation offers better coverage of gram –ve bacilli.
 Antipseudomonal cephalosporins: Ceftazidime, Cefepime
 Ceftaroline has activity against MRSA and gram negative but not against Pseudomonas. Approved for
Complicated skin infection and community acquired pneumonia.
Carbapenems (Imipenem): It also inhibits synthesis of bacterial cell wall. Also has cross reactivity with
penicillin allergic patients.
 It is one of the broadest spectrum antibiotic including Pseudomonas.
 It is always used with Cilastatin (Imipenem-Cilastatin). Cilastatin inhibits the dehydropeptidase found in
the brush border of proximal renal tubule. This enzyme can metabolize Imipenem to a nephrotoxic
metabolite. Cilastatin helps in two ways. 1. Prevents nephrotoxicity 2. It allows drug to be active in the
treatment of urinary tract infection.
 S/E: Seizure.
Monobactum (Aztreonam): It is active only against gram negative rods. It is not effective against gram
positive and anaerobes.

Vancomycin: Also inhibits bacterial cell wall synthesis as beta lactam antibiotics.
 Mainly used for gm+ve
 Treatment of choice for MRSA (Methicillin Resistant Staph. Aureus)
 MRSA is due to alteration of PBP (Penicillin binding protein in the bacterial cell wall). Due to the
alteration it requires very high concentration of the drug to have effective binding, which is practically
not possible. It occurs in Staph aureus with mec gene. Staph aureus without mec genes are susceptible to
Methicillin. Mec gene alters the protein binding protein 2a.
 VRSA/VRE (Vanco resistant staph aureus/Vaco resistant enterococci): It is due to plasmid mediated
transfer of VanA gene cluster which replace cell wall terminal peptide (D-ala-D-ala) to (D-ala-D-lac).
Vancomycin is unable to bind to (D-ala-D-lac) peptide.
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 Plasmid is a DNA molecule found in bacteria that is separate from chromosomal DNA, and can replicate
independently. Plasmids may carry genes, which cause resistance to antibiotics and can transfer it to
other bacteria.
 S/E: Redman Syndrome, if administered rapidly.
Daptomycin: causes depolarization of the bacterial cell membrane.
 Used for MRSA
 Not effective to treat MRSA pneumonia
 S/E: Myopathy, Peripheral Neuropathy
Antibiotics used for Vancomycin Resistant Enterococci (VRE)-
 Linezolid (zyvox), Quinupristin- Dalfopristin (synercid), Tigecycline
 They are also effective for MRSA
 Side effects of Linezolid: Thrombocytopenia, Serotonin syndrome especially in patients on SSRI,
Peripheral neuropathy, Lactic acidosis
Tigecycline: Derived from minocycline
 Effective against many gram positive (Including MRSA and VRE), many gram negative (Except
Pseudomonas and proteus), anaerobes and atypicals

Macrolides: Inhibits bacterial protein synthesis


 Erythromycin, Clarithromycin, Azithromycin
 Drug of choice for Legionella and Mycoplasma
Clindamycin: Inhibits bacterial protein synthesis
 Good gram +ve & anaerobic coverage.
 S/E: Pseudomembranous colitis.

Aminoglycoside: Inhibits bacterial protein synthesis


 Mainly used for gm –ve bacilli
 Another important indication is for synergistic effect with penicillin and vancomycin for the treatment of
enterococci and streptococci in endocarditis.
 S/E: Nephrotoxic- after 5 days of use
Ototoxic: after 14 days of use.
Fluoroquinolones: Inhibits replication of bacterial DNA by interfering with the action of DNA gyrase
 Ciprofloxacin, Levofloxacin, Gatifloxacin, Moxifloxacin, Norfloxacin
 Covers most gm+ve, -ve including Pseudomonas
 Avoid in children and pregnant and breast feeding woman.
Causes: Cartilage erosion and non inflammatory effusion in the weight bearing joints of children.
Metronidazole
 Treatment of choice for Pseudomembranous colitis, Giardia, Entamoeba histolytica
 S/E: Metallic taste, disulfiram like reaction with alcohol.
Anti-tuberculous drug- Side Effects
 INH- hepatotoxic, Peripheral neuropathy (Add Pyridoxine to prevent)
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 Rifampin- Hepatotoxic
orange red discoloration of urine & sweat- no need to stop the treatment.
 Ethambutol- decreased Red-Green color perception, decreased visual acuity and visual field.
 Pyrazinamide- hyperuricemia- (comes with attack of gout), Hepatotoxic

Antiviral
 Acyclovir (Inhibits viral replication by interfering with viral DNA polymerase)- nephrotoxic secondary
to precipitation into renal tubules- to prevent well hydrate the patient
 Ganciclovir- Neutropenia- reversible
 Foscarnet- Nephrotoxic

Antifungal
 Amphotericin B- Binds to ergosterol which alters cell membrane permeability in susceptible fungi and
causes leakage of cell components with subsequent cell death. Causes Nephrotoxicity, Hypokalemia,
hypomagnesemia-secondary to loss in urine.
Prevention: IV hydration
 Voriconazole: Interferes with fungal cytochrome P450 activity, decreasing ergosterol synthesis
(principal sterol in fungal cell membrane) and inhibiting fungal cell membrane formation. “Same like
other Azoles”. Approved for invasive aspergillosis- Can cause visual changes (Blurred vision,
photophobia)
 Caspofungin: Inhibits synthesis of ß (1,3)-D-glucan, an essential component of the cell wall of
susceptible fungi. Approved for invasive Candidiasis-usually well tolerated can cause elevation of
transaminases

Sexually Transmitted Diseases


 Gonorrhea
 Chlamydia
 Syphilis
 Chancroid
 Genital Herpes
 HIV
 Lympho granuloma venerum
 Granuloma inguinale

Gonorrhea / Chlamydia
 In gonorrhea, discharge per urethra is purulent. In Chlamydia, mucoid or watery.
Investigation:
 Gonorrhea Gram stain (Gram –ve Intracellular diplococci), DNA probe, Culture (Using Thayer Martin
Medium is Gold standard), Nucleic acid amplification (NAAT) {using either Polymerase chain reaction
(PCR), Transcription mediated amplification (TMA), or Standard displacement amplification (SDA)
provides rapid results but very expensive, although it is most sensitive and specific test for N.
gonorrhoeae and is recommended by the Centers for Disease Control and Prevention. Another advantage
of NAATs is the ability to perform testing on urine as well as urethral specimens}.

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 Chlamydia Genetic Probe (mostly used), Culture (Rarely used as requires tissue culture), Nucleic acid
amplification (NAAT) {Gold standard, using either Polymerase chain reaction (PCR), Transcription
mediated amplification (TMA), or Standard displacement amplification (SDA)}, Antigen detection.
Treatment:
 Ceftriaxone 125 mg IM one dose + Doxycycline 100 mg PO BIDx 7 days.
or
 Ceftriaxone IM + Azithromycin 1gm PO (DOC for pregnant pt.) “Preferred t/t by pts.”
 {Ceftriaxone for Gonorrhea and Doxy or Azithromycin for Chlamydia}
 Alternative treatment for Gonorrhea: Oral cefixime or Oral 2 gram Azithromycin or spectinomycin
 Penicillin Allergic patients- instead of Ceftriaxone give Spectinomycin IM (Can be used in pregnancy)
 Pregnant pt.: Ceftriaxone IM + Instead of Doxycycline use Erythromycin Base or Azithromycin or
Amoxicillin
 Currently spectinomycin is not available in USA (Available outside USA) and CDC discourages use of
Azithromycin for Gonorrhea as concerned about rapid resistance. So in patients allergic to penicillin may
be the only option at present is desensitization with cephalosporin. Although CDC is working with drug
companies to make Spectinomycin available.
 Try to treat pt. sexual partner also to prevent reinfection

END OF 1ST HOUR


Primary Syphilis
 Caused by Spirochete, Treponema Pallidum
 Lesion begins as painless papular lesion on genitalia, which later on ulcerate to produce ulcer with
raised, indurated margin called chancre. Chancre is usually single associated with painless inguinal
lymphadenopathy, with firm rubbery consistency. If this ulcer is not noticed, heals spontaneously in
three to six weeks without treatment.
 Investigation: Dark field microscopy (serologic test may be negative in 30% patients)
 Treatment: Benzathine Penicillin 2.4 million unit IM X1 dose or Doxycycline PO X 2 week.

Secondary Syphilis
 Usually if primary syphilis is untreated, 25% of patients develop secondary syphilis in weeks to months.
 C/F- Rash generalized maculopapular including palm and sole, generalized lymphadenopathy,
elevated liver enzymes, alopecia, Condyloma lata- Flat, velvety, gray to white lesion in perineal area.

Investigation:
 Serological Test:
 Non Treponemal- VDRL (Venereal disease research laboratory test), RPR (Rapid Plasma Reagin test)
Preferred, as inexpensive.
 Treponemal test- done if non treponemal test is positive, as this is more specific and confirmatory test.
Once positive, remains positive for most of the patients.
 Florescent Treponemal antibody absorption test (FTA-ABS)
 Microhemagglutination test for antibodies to Treponema Pallidum (MHA- TP)
 Treatment- Benz. Penicillin 2.4 MU IM x 1 dose or Doxycycline x 2 weeks

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 Differentiate Condyloma lata from Condyloma Accuminata (Ano-genital wart)- Caused by Human
Papilloma Virus, these are skin colored, flesh color, or pink, verrucous, papilliform, cauliflower like
lesion in the perineal area, lesions are painless
 Diagnosis is clinical. Application of acetic acid can turn lesions white. Biopsy can be done if diagnosis
is in doubt.
 Treatment of C. Accuminata-
 Podophyllin (25%)-Contraindicated in pregnancy
 Trichloroacetic acid-First line of treatment in pregnancy
 Cryotherapy with liquid nitrogen can also be used as first line therapy, if available. It is safe in
pregnancy.
 Imiquimod (Local interferon) 5% cream-Less pregnancy risk (Category B) than podophyllin (Category
X)
 Snip biopsy (Scissors) followed by light electrocautery
 If above fails, laser therapy or surgical excision (especially if very large lesion).
Jarisch Herxheimer reaction
 Usually after two hours of treatment for primary and secondary syphilis and 12 hours after treatment of
neurosyphilis. Patient may develop fever, chills, headache secondary to release of lipo-polysaccharide
from dying spirochetes.
 Treatment; Bed rest, Aspirin.

Patients with latent syphilis should have CSF examination done if anyone of the following is present.
1: Ophthalmic signs of syphilis
2: Other evidence of active tertiary syphilis
3: Treatment failure
4: HIV infection if latent syphilis more than one year duration or unknown duration

Causes of false positive serologic test of syphilis


 SLE (Systemic Lupus Erythematosus)
 Intravenous drug abuse
 Chronic liver disease
 HIV

Causes of false negative test of syphilis


 In primary syphilis, 30% patients may have negative serology, as antibodies may not have developed.
 Prozone reaction: Affects non treponemal test only and is due to high titer of antibody
(Mismatch between concentration of antigen and antibody)

Treatment of syphilis follow up:


 Treponemal test- once positive remains positive for life for most patients.
 Non-Treponemal test: Monitor titer
 For primary and secondary syphilis, titer should decrease four fold in six months and eight fold in 12
months.
 In latent and neurosyphilis, titer should decrease by four fold in 12 months.

Chancroid

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 Painful genital ulcer with soft and necrotic base with painful lymphadenopathy. Inguinal lymph node
may undergo liquefaction and present as painful, fluctuant bubo.
 Caused by Hemophilus ducreyi (Gram negative rod, in gram stain, has school of fish appearance)
 Treatment: Azithromycin 1 gm PO X one dose or Ceftriaxone- 250 mg IM X one dose

Genital Herpes
 Cause: HSV type2
 C/F: Multiple, small, painful, shallow ulcers in genital area. In early lesions it could be vesicular, painful
lesion on erythematous base. May have Bilateral tender inguinal lymphadenopathy.
 Confirm with:
Tzank preparationmultinucleated giant cells
Culture
PCR
 T/t: Acyclovir, Valacyclovir, Famciclovir ↓duration of symptoms and viral excretion time
 Acyclovir resistance: Increasing incidence in immunocompromised patient (HIV, Transplant)T/t:
Foscarnet I.V.
 When lesions are present even if condom is used transmission is possible.
 Transmission is possible during asymptomatic period
 Usually patient is once infected, have latent infection which can be reactivated secondary to fever,
trauma and immunodeficiency
 Recurrent infections (if > 6 episode / yr) can be treated with daily suppressive therapy, to decrease
frequency of reactivation

Lympho-granuloma Venerum (LGV)


 Usually present with B/L large, tender inguinal lymph node with draining sinuses
 Initial genital lesion, which is painless, usually not noticed and pt. mostly present with above finding.
Perirectal glands may be involved in women or homosexual men and present with Proctitis, rectal
stricture, rectovaginal or perirectal fistula.
 Groove Sign: Another characteristic sign, It is inflammatory reaction in the superficial and deep inguinal
lymph nodes.
 Cause: L1, L2, L3 chlamydia trachomatis
 Treatment: Doxycycline

Granuloma Inguinale
 Present with painless large ulcerated lesion in genital area with beefy-red friable base of granulation
tissue.
 Cause: Calymmatobacterium granulomatis
 Lab: Tissue scraping or secretion contain Donovan bodies.
 T/t: Tetracycline or Erythromycin

Genital ulcers
 Syphilis ulcer is painless with clear base and raised, indurated margin, with painless lymphadenopathy.
 Chancroid Painful, deep, ulcer with purulent base, associated with painful lymphadenopathy
 Genital herpes Multiple, shallow painful ulcer, usually vesicular as initial lesion

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 LGV Painless, small and shallow lesions mostly not noticed and patient presents with bilateral large,
tender inguinal lymphadenopathy, often associated with sinus tract.
 Granuloma inguinale Large, ulcerated, painless lesion with beefy red friable base of granulation tissue.
END OF 2nd HOUR
HIV
Risk factors:
 Unprotected sex with multiple sexual partners.
 Homosexual (more risk than heterosexual but still the majority of spread occurs by heterosexuals)
 Needle sharing
 Infected blood transfusion
 Perinatal exposure

Risk of Acquiring infection


 Blood transfusion 1:100,000
 Needle stick 1:300 (0.3%)
 Perinatal( child born to HIV infected mother) 13-40%

Needle stick transmission


 HIV- 0.3%
 Hep C-3% (0-7)
 Hep B- 30% (6-30)
 After needle stick from HIV patient. Immediately with in 1-2hr start Triple therapy:
AZT+3TC+Indinavir for 4weeks. It decreases transmission 75%
Investigation
 Screening test- ELISA
 Confirmatory Test- Western Blot
 Viral Load- HIV RNA PCR
 Newborn of HIV mother: Test of choice is “HIV DNA PCR”. ELISA or Western blot is not
recommended as maternal antibodies persist for few months in infants. If these test are positive after 18
months indicate infection. HIV RNA PCR can also be undetectable in new born if mother was getting the
treatment.
 CD4 count -
< 350 cells/µl indicates need of treatment (More than 350 cell could also be started based on comorbidities
and patient readiness for the treatment. Presence of active hepatitis B or C virus coinfection,
cardiovascular disease risk, and HIV-associated nephropathy prompt earlier therapy)
< 200 cellStart Prophylaxis for Pneumocystis Jiroveci Pneumonia (PCP)Bactrim-drug of choice or
Dapsone or Aerosolized Pentamidine or Atovaquone
< 100 cellsToxoplasma prophylaxis (If patient is Toxo IgG +ve): Bactrim or Dapsone + Pyrimethamine+
leucovorin
<50 cellsStart Mycobactrium Avium Complex Prophylaxis (Azithromycin 1200mg Q weekly or
Clarithromycin 500mg BID)
<150 cellsHistoplasma prophylaxis (If patient lives in endemic area): Itraconazole
 P24 antigen
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 Pancytopenia
Rapid Screening test for HIV
• Results are available in minutes and sensitivity and specificity of these test are >99%
• Rapid test are preliminary and require confirmation with ELISA and Western blot, but if negative, no
further testing required, except in patients who are in window period of acute HIV infection. In these
patients test should be repeated after 12 weeks of exposure.
• It is a serology test, 4 types of test approved by FDA are: Oraquick Rapid HIV -1 antibody test, Uni-
gold Recombigen HIV test, Reveal HIV-1 antibody test, Multispot HIV-1/HIV-2. In Oraquick saliva
also can be used as specimen
These tests are especially used for:
• Patients unlikely to return for result. Upto 40% of patients do not return for result.
• Women present in labor without prior testing.
• After acute (Occupational or non-occupational) exposure. {Serologic status is very important to know
before starting antiretroviral prophylaxis.}
Aerosolized Pentamidine
 Less effective in apical areas of lung: so patient can have apical PCP (Pneumocystis Jiroveci
Pneumonia) while on treatment
 Increased incidence of Pneumothorax if patient has h/o PCP
 If someone on Aerosolized Pentamidine gets PCP Prophylaxis after treatment will be Bactrim or
Dapsone.
Health Maintenance - HIV Patients
 Pneumococcal vaccine at diagnosis then repeat after 5 years
 Influenza vaccine annually
 Hepatitis B vaccine: If Hep B surface antigen and antibody –ve.
 Hepatitis A vaccine: If Hep A IgG antibody –ve.
 MMR and Varicella: can be given if CD4 > 200 or CD4 +T lymphocyte is >15% of total lymphocyte
 PPD annually, if –ve. If +ve and has been treated for 9 month with INH chest X-ray annually.
 Pap Smear- every six months in first year then annually.
Vaccinations Contraindicated in HIV
 OPV (Oral Polio Virus)
 Yellow Fever
 MMR & Varicella- if CD4 < 200 or CD4 +T lymphocyte is <15% of total lymphocyte
Antiretroviral Therapy
• Nucleoside and Nucleotide reverse transcriptase inhibitor: Zidovudine (AZT), Didanosine (DDI),
Zalcitabine (ddc), Stavudine (d4T), Lamivudine (3TC), Abacavir, Tenofovir, Emtricitabine, Combivir
(AZT+3TC), Truvada (Tenofovir + Emtricitabine)
• Non-Nucleoside reverse transcriptase inhibitor- Nevirapine, Delaviridine, Efavirenz
• Protease inhibitor: Saquinavir, Ritonavir, Indinavir, Nelfinavir, Amprenavir, Lopinavir/Ritonavir
(Kaletra), Atazanavir, Darunavir, Fosamprenavir, Tipranavir
• Fusion Inhibitor: Enfuviritide (Peptide T-20) it blocks entry of HIV into cells. It is available only in
subcutaneous injection form. Used for multi drug resistant HIV
• CCR5 Inhibitor: “Maraviroc” It is another entry inhibitors
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• Integrase Inhibitor: “Raltegravir” It inhibits viral replication
• Most commonly used combination: 2 nucleoside +1 non nucleoside or 2 nucleoside +1 protease
inhibitor
• Nucleoside +Protease inhibitors combination has been linked to cause lipodystrophy {Elevated
cholesterol and triglyceride level, insulin resistance, diabetes and changes in body fat composition
(Abdominal obesity and skeletal wasting)}
• Protease inhibitors are metabolized by the cytochrome P-450 system. When treating increased LDL
cholesterol use Pravastatin, Fluvastatin and Rosuvastatin (Atorvastatin if above drugs not available).
Avoid using lovastatin, simvastatin. Avoid using lovastatin, simvastatin. If triglyceride level is
>500mg/dl treat with Gemfibrozil.
• Lamivudine, Tenofovir and Emtricitabine also has activity against hepatitis B

Combinations of Antiretroviral
 Combination not acceptable: Zidovudine (AZT)+ Stavudine (d4T)Antagonist
 Combination Avoided:
DDI+DDC Same S/E
AZT+GanciclovirSevere Bone Marrow suppression
Stavudine+Didanosine in pregnant pt.↑ risk of lactic acidosis
Indications to start treatment
• CD4 <350
• HIV with symptomatic disease
• Pregnancy
Indication of changing combination therapy
 Intolerance to medication
 Progression of disease- decreasing CD4 count, increasing viral load
 Less than 1 log reduction of viral load by 4 weeks of starting therapy.
Side Effects of Antiretroviral
 AZT- macrocytic anemia (↑MCV), Neutropenia, myopathy
 DDI, ddc, d4T, 3TC- Peripheral neuropathy
 DDI- Pancreatitis
 Abacavir-Hypersensitivity syndrome: Flu like symptoms with rash and fever.
 Tenofovir- Acute renal Failure, Fanconi Syndrome
 Nevirapine- Liver toxicity, rashes including toxic epidermal necrolysis and Stevens-Johnson syndrome
 Efavirenz- Neurologic disturbance- presents with change in mental states. Avoid in patients with seizure
disorder. Teratogenic so avoid in patient with child bearing age.
 Indinavir- Kidney stone
 Nelfinavir- Diarrhea
 Stavudine: Progressive ascending neuromuscular weakness (Like Guillain Barre syndrome)
END OF 3rd HOUR
CNS enhancing lesion in HIV patients
 Toxoplasmosis
 CNS lymphoma
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 Brain abscess- easily differentiated in CT and MRI

Toxoplasmosis
 All HIV patients should be screened for toxo IgG and if positive should be on prophylaxis once CD4
<100.
 Usual presentation is Headache or Weakness of extremities or Change in mental status, in a patient
usually not on prophylaxis, CD4<100, MRI or CT head shows ring enhancing lesions.
 Other D/D is Lymphoma, which needs brain biopsy to confirm the diagnosis.
 Usually toxo is multiple lesions and lymphoma is single.
 Once suspect toxo, start treatment empirically:
 Sulfadiazine+Pyrimethamine+leucovorin
 If sulfa allergic: Clindamycin+Pyrimethamine+leucovorin
 Reevaluate lesion after 2 weeks of treatment by another MRI or CT. If lesion has diminished in size
continue the treatment for 4-8 weeks, otherwise arrange for brain biopsy.

CNS nonenhancing demyelinating hypodense lesion in white matter


 Progressive multifocal leukoencephalopathy (PML)
 Cause: JC virus
 C/F: Hemiparesis, cortical blindness
 Treatment: Antiretroviral therapy

Cryptococcal meningitis
 HIV pt with c/o fever, headache, CT head negative (r/o toxoplasma)
 Investigation: crypt antigen +ve in blood and CSF.
 CSF with India ink shows encapsulated yeast.
 Treatment: Amphotericin B + Flucytosine.
CMV Retinitis
 C/F- HIV patient c/o blurring of vision
 Ophthalmoscopy: Perivascular hemorrhage and fluffy exudates.
 Treatment: Ganciclovir (s/e- Neutropenia: avoid with AZT)
Valganciclovir (diff. from ganciclovir is↑ oral bioavailability)
Cidofovir: Nephrotoxic
Foscarnet: Nephrotoxic, Hypocalcemia

HIV patient with centrally umblicated papular (dome shaped) lesion on the skin.
 D/D: Molluscum contagiosum and cryptococcosis
 Lab: cryptococal antigen and skin biopsy
 Treatment of Molluscum Contagiosum: Curettage or cryotherapy with liquid nitrogen
 Treatment of cryptococcosis: Fluconazole

HIV patient with papular reddish vascular lesion


 Bacillary angiomatosis: usually with fever
Caused by Bartonella henselae, Bartonella Quintana.
Confirmed by Biopsy
Treatment: Doxy or Erythromycin
 Kaposi’s sarcoma: not a cause of fever
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Most common HIV related malignancy
Other associated lesion on hard palate and pulmonary nodule
Confirmed by biopsy
Treatment: Vincristine, Vinblastine, Alfa interferon

HIV Patient with White Lesion on the Tongue


 Hairy leukoplakia:
Usually on the lateral aspect of tongue can not be removed on scraping
Treatment: Acyclovir
 Oral Candidiasis:
Usually involves oral mucosa also and easily removed on scraping.
Treatment: Clotrimazole troches or Nystatin swish and swallow. If not improved, oral Fluconazole.

HIV Patient with Dysphagia


If patient has oral thrush - treat empirically with oral Fluconazole for 2 weeks, if symptom does not improve
then Endoscopy.
Endoscopic findings:
• Esophageal Candidiasis: diffuse white lesion T/t: Fluconazole
• Herpes simplex: deep, small, multiple lesion T/t: Acyclovir
• CMV: superficial large lesion. T/t: Ganciclovir
Note: other immunocompromised patients like leukemia, lymphoma on chemotherapy will have same D/D
for dysphagia.

HIV Patient with Diarrhea


 Besides other tests usually done in a normal patient order acid fast staining of stool for ova and parasite
to diagnose
 Cryptosporidia- T/t: Nitazoxanide or Paromomycin
 Cyclospora or Isospora: T/t: Bactrim
 If stool work up, negative colonoscopy shows ulcers or erosions in colon, biopsy shows- large cells
containing a basophilic intranuclear inclusion, which is sometimes surrounded by a clear halo ("owl's
eye" effect) and is frequently associated with clusters of intracytoplasmic inclusions  CMV colitis.
Systemic Fungal Disease
 Sporotrichosis
 Coccidiodomycosis
 Cryptococcosis
 Histoplasmosis
 Blastomycosis
Sporotrichosis
 Caused by Sporothrix Schenckii
 Usually after thorn pricks to a gardener.
 Hard, non tender, subcutaneous nodules along the lymphatic drainage
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 Treatment: Itraconazole (doc)
 If HIV patient or systemic disease - Amphotericin B.
Coccidiodomycosis
• Travel history of New Mexico, Arizona, Central California, West Texas, Mexico, Central and South
America
• Infection results from inhalation of the organism, causing pulmonary infection
• Even brief exposure is sufficient to cause infection
• M/C presenting symptom is fever, cough, pleuritic chest pain and often misdiagnosed as community
acquired pneumonia
• Arthralgia (Also called desert rheumatism)
• Erythema Nodosum or erythema multiforme
• Chest X-ray: multiple nodular lesion, w/ cavity (Initial X-ray may be normal or have unilateral infiltrate)
• Serology: Antibody, coccidioidomycosis
• Sputum for fungal stain and culture
• Sputum may have spherules containing endospores
• Treatment: In less severe: Itraconazole or Fluconazole
In severe case: Amphotericin B
• Risk Factors: HIV, Transplant Patient, Lymphoma, Diabetes, Pregnancy, Patients on Prednisone
>20mg/day, Anti-tumor necrosis factor therapy
Cryptococcosis
 Patient with HIV, Hodgkin’s disease, on steroid (immunocompromised patient)
 Most common cause of fungal meningitis
 C/F: headache, change in mental status.
 Investigation: India ink +ve
 Cryptococcal antigen in CSF, C/S of CSF.
 Treatment: Amphotericin B +Flucytosine
Histoplasmosis
 Most prevalent endemic mycosis in the united states
 Ohio River, Mississippi River valley
 Soil contaminated with Bird dropping, Bat exposure, mostly affected are immunocompromised people.
 History of exposure to chicken coops, bird roost sites, farm house w/ a lot of chicken droppings,
abandoned buildings, caves, wood lots.
 Usually present with cough, SOB
 Hepatosplenomegaly, lymphadenopathy, oral ulcer
 Investigation: Urine and Serum for Histoplasma antigen, Histoplasma complement fixation test, fungal
C/S, Pancytopenia, increased liver enzymes and increased LDH level
 CXR: Pulmonary infiltrate
 T/t: Amphotericin B, Itraconazole
 In HIV patients, after treatment with Amphotericin B, will be on Itraconazole for maintenance.
 In pregnant patient, Amphotericin B is the drug of choice, Itraconazole is contraindicated.
Blastomycosis
 Midwest, South Central
 Had outdoor activity
 Raised verrucous lesion with central atrophic scar
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 Most commonly presents with involvement of skin and urogenital system
 A wet mount preparation shows multinucleate yeast cell with thick refractile cell wall.
 T/t: Itraconazole- if does not respond Amphotericin B.
Invasive Candidiasis
 Risk Factors: Central venous catheter, Total Parenteral nutrition, Corticosteroid therapy, Neutropenia,
Broad spectrum antibiotic therapy
 Risk of developing candida endophthalmitis and loss of vision, endocarditis, multiorgan involvement
 Remove all the catheters
 Start Fluconazole
 In institution where candida glabrata or candida krusei is common, patients who have been on
fluconazole prophylaxis, unstable patients, neutropenic patients Caspofungin should be used. Alternative
drug is Amphotericin B
Nocardiosis
• Mainly caused by Nocardia asteroides
• Lungs are primary site of infection
• Since upper lobe involvement is common, and Nocardia is weakly acid fast, often misdiagnosed as
Tuberculosis
• Clinical Features: Fever, night sweats, weight loss, cough, dyspnea, hemoptysis, pleuritic chest pain in
immunocompromised patients (HIV, Transplant patient, Malignancy on chemotherapy, on steroid
treatment)
• Diagnosis: Demonstration of partially acid fast, filamentous, branching, gram positive rods
• Culture: Blood or sputum culture- should be held for four weeks
• Chest x-ray single or multiple nodules, lung mass (with or without cavitations)
• Treatment: Trimethoprim- sulfamethoxazole (Drug of choice)
• Patient allergic to sulfa Amikacin or Imipenem or third generation cephalosporin
• Not responding to antibiotic surgery

Actinomycosis
 Cervicofacial involvement is most common manifestation of Actinomycosis, primarily caused by
Actinomyces Israeli
 Characterized by abscess formation, draining sinus tract, fistula. Most easily recognized manifestation is
fistulization from perimandibular region, also called “ lumpy jaw”. Mostly after trauma, surgery, dental
caries, poor oral hygiene
 Gram positive filamentous bacteria. Exudates from sinus tracts often contain sulfur granules (yellowish
green calcified structure)
 Not a contagious disease
 Treatment: Penicillin (DOC), (If allergic Tetracycline, Erythromycin, Clindamycin) and surgical
drainage.
Mucormycosis
 Usually patients are immunocompromised
 Most common organism is Rhizopus
 Diabetic, CRI, on steroid, on cytotoxic drugs
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 C/F: symptoms mostly secondary to invasion into sinuses or orbit, Bloody nasal discharge with black
necrotic lesion of nose or double vision with reduction of movement of eye (sec. to cranial nerve
involvement and invasion of ophthalmic artery)
 Investigation: CT, MRI shows opacification, Biopsy shows hyphae broad, irregularly branched with rare
septation.
 Treatment: Surgical debridement (Main treatment)+ Ampho B IV, tight control of diabetes
END OF 4th HOUR
Diseases Transmitted by Ticks
 Lyme disease
 Babesiosis
 Ehrlichiosis
 Rocky Mountain spotted fever
Lyme Disease
 Caused by Borrelia Burgdorferi
 Transmitted by Tick bite (Ixodes scapularis)
 Patient from Massachusetts (Nantucket), Connecticut, Maine, New Hampshire, Rhode Island, New York
(Long Island, Westchester), New Jersey, Pennsylvania, Delaware, Maryland, Michigan, and Wisconsin
(tick endemic region)
 Patient might not recall tick bite.
 Erythema chronicum migrans: erythmatous rash on groin, thigh, axilla- gradually enlarging with central
clearing- disappear in few days. Treatment in this stage: Doxy
 After few days or weeks comes with dizziness found to have
first degree AV block: T/t: Doxy.
2nd or 3rd degree AV block: T/t Ceftriaxone
Comes with Bells palsy or foot drop: T/t: Doxy
Comes with symptoms of meningitis: T/t: Ceftriaxone
 After months to year later comes with arthritis- T/t Doxy
 Doxy should be avoided in children < 8 years of age and pregnant patient Amoxicillin (Penicillin
allergic Macrolides: eg Azithromycin)
 Diagnosis is clinical in early lyme disease
• For late disease: ELISA  Western Blot
Lyme Disease Transmission:
 Risk is very low:
1: If tick was removed in less than 48 hours {Usually Borrelia is in the gut of Ixodes, after feeding blood
the number of Borrelia starts multiplying and after 48 hours, migrates to the salivary gland. (This period
is not required for organisms causing Ehrlichiosis (Anaplasma Phagocytophilia) and Babesiosis
(Babesia microti), they are already present in Salivary gland)}
2: If tick removed was not engorged (After blood meal, tick becomes large and globular)

Prophylaxis after tick bite:


• 1: Low risk patients: Antibiotic prophylaxis is not recommended. Patient should be educated and
observed for development of erythema migrans at bite site in 30 days. (Transient erythema may develop
in 24 to 48 hours at the site of bite secondary to reaction to tick saliva) The only exception is pregnant

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patient where the risk is low, but get prophylactic treatment since the anxiety level is very high 
Amoxicillin 500mg TID X 10- 14 days.
• 2: High risk patients, if patient has been bitten in an area, where incidence of lyme is very high and tick
removed was engorged or attached for > 48 hours Doxy 200 mg single dose.

Babesiosis
 Patient from tick endemic areas comes with fever, chills, drenching sweats, no rash.
 On peripheral smear small ring form in RBC
 Treatment: Atovaquone + Azithromycin

Ehrlichiosis
 Patient from tick endemic area comes with fever, headache, h/o tick bite
 Leukopenia, thrombocytopenia
 Treatment: Doxy

Rocky Mountain spotted fever


 Patient from tick endemic region comes with c/o fever, headache, on 4th day developed macular rash on
wrist, palm, ankle and feet (distal extremity) which after one to two days becomes petechial
 Treatment: Doxy

Young Children with Rash


 Roseola infantum
 Erythema infectiosum
 Measles
 Rubella
 Scarlet Fever
 Varicella

Roseola Infantum (Exanthem Subitum)


 Characteristic history of fever for 3-4 days when patient becomes afebrile: developed-maculopapular
rash
 Cause: Herpes virus 6
 Treatment: self limited

Erythema infectiosum (fifth disease)


 Young child with rash on cheeks has “slapped cheek appearance”, on the body rash with reticular
pattern, lace like rash
 Cause: Parvovirus B19
 Note: Patient with this disease are infectious only before the rash appears- so if a child comes with rash
diagnosed as fifth disease can go back to school.
 Pregnant patient exposed to patient with Parvovirus B19 infection have risk of fetal loss or hydrops
fetalis.

Measles (Rubeola)
 Cough, coryza, conjunctivitis, photophobia, Koplik’s spot (small red spot with gray or white center on
the buccal mucosa)

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 Fever with brick red maculopapular rash begins on face spread downward (Koplik’s spot disappear
when rash appear)
 Complication:
Subacute sclerosing panencephalitis, Pneumonia

Rubella (German Measles)


 Mild fever
 Posterior cervical and post-auricular lymphadenopathy 5-10 days before rash.
 Maculopapular rash begins on face spread downward.
 Congenital Rubella syndrome: deafness, cataract, congenital heart disease (PDA), mental retardation,
microcephaly.

Scarlet fever
 Erythematous rash that blanches on pressure
 Circumoral pallor
 Strawberry tongue
 Skin rough feel like sand paper
 Cause: Group A streptococci.

Varicella (Chicken Pox)


 Rash begins as papule vesicle pustule scab.
 Rash: Pruritic, centrifugal (begins on trunk spread peripherally)
 Rash: appear in crops so that several stages of lesion present at the same time.
 Highly contagious- air borne isolation till all lesion are crusted (usually 8-21 days)
 Complication:
Bacterial skin infection (Most common in patients <19 yrs of age)
Pneumonia (Most common in patients >19 yrs of age)
Encephalitis- characterized by ataxia and nystagmus
Reye’s Syndrome: with aspirin.
Treatment:
 Children <12 years old:
HealthySupportive treatment (Acetaminophen, Antihistamine), no acyclovir
Neonates or Immunocompromised IV acyclovir
 Children >12 years old or Adult: Oral Acyclovir

Post Exposure prophylaxis:


Healthy Person:
 Immune: Nothing to worry
 Not immune: Varicella vaccine with in 3-5 days (It may be protective)
Immunosuppressed or Pregnant women:
 Immune: Nothing to worry
 Not Immune: VariZIG Intramuscular
Herpes Zoster (Shingles)
 Reactivation of Varicella
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 Usually starts with burning type pain in affected nerve, a single unilateral dermatome is involved
(On right or left side of trunk it will not cross the midline “band like”). In the face only one side of face.
 After pain vesicular lesions appear on the same dermatome
 Tzanck Test: Scraping from base of the vesicle demonstrate- multinucleated giant cell with intranuclear
inclusion (+ve in varicella and Herpes simplex also)
 Ramsay Hunt Syndrome: Facial Palsy, zoster Lesion of external ear, vertigo, tinnitus and deafness
 T/t: Acyclovir, Famciclovir, Valacyclovir- decreases severity and duration of lesion and incidence of
post herpetic neuralgia.
 If eye involvedrefer immediately to the ophthalmologist.
 Post herpetic neuralgia: severe pain at the site of shingles after healing.
Treatment: Amitriptyline, opioids, topical capsaicin, gabapentine.
Herpes Simplex
 Type 2: involve genital tract
 Type 1: herpes labialis- group of vesicle around mouth usually recurrent- precipitated by stress, fever,
infection, chemotherapy
 Complications: Bell’s palsy, encephalitis, ocular lesion
 Treatment: Acyclovir
Parvovirus B19 and Pregnancy
 Pregnant patient exposed to patient with Parvovirus B19 infection have risk of fetal loss or hydrops
fetalis
 Patient exposed should be tested for B19 IgG and IgM level. Those with IgG are immune but if IgM
present suggest acute infection. It takes 10 days after exposure for IgM to be positive
 Patient with IgM positive and less than 20 weeks of pregnancy should be told about the risk of fetal loss
and fetal hydrops. No action needs to be taken prior to 20 week. From 24 weeks onward, weekly
ultrasound is recommended to look for fetal hydrops (Ascites, scalp edema, polyhydramonios,
cardiomegaly) and if develops refer to tertiary care center for the management.
 Pregnant patient with high risk employment like school teacher or day care center worker have no
recommendation to leave the job.
Infectious mononucleosis
 Caused by Epstein Barr virus
 C/F: Fever, sore throat, lymphadenopathy, splenomegaly, Palatal petechiae
 Labs: Lymphocytic leukocytosis, Atypical lymphocyte (Large basophilic cells with vacuolated
appearance), Heterophil antibody (Monospot) test +ve
 Avoid Physical activity: especially contact sports for one month till splenomegaly resolves either on
examination or by ultrasound, to avoid splenic rupture.
 If misdiagnosed and treated with ampicillin Rash (another way to diagnose Infectious mononucleosis)
 Treatment: supportive
Sore Throat
 Strep. Infection
 Infectious mononucleosis
 Diphtheria
 Peritonsillar abscess
 Viral illness
 Epiglottitis
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END OF 5th HOUR


UTI (Urinary Tract Infections)
Cystitis:
 Usually young sexually active female with increased frequency of urine, dysuria, may have lower
abdominal discomfort No further test is required. Start treatment empirically for 3 days with either
Bactrim (Trimethoprim-Sulfamethoxazole) or Ciprofloxacin. If patient is still symptomatic after 3 days
requires urine culture.
 If patient is Pregnant or Male patient, requires urine analysis, urine culture and antibiotics are used for 7
days.
 In pregnant patient use Amoxicillin, if allergic to Penicillin use Nitrofurantoin.
 Male patients should always be worked up for cause of UTI.
 Most common organism is E. coli but if urine pH is alkaline about 8.0 likely organisms would be
Proteus (Produces Urease)

Pyelonephritis:
 Clinical Features: Fever, polyuria, dysuria, flank pain, may have nausea, vomiting, on exam
costovertebral angle tenderness present
 Investigation: U/A, Urine culture
 Treatment: Ciprofloxacin for 10-14 days
 In pregnant patient antibiotic of choice is Ampicillin + Gentamicin IV if allergic to penicillin use
Aztreonam or Imipenem
 Once patient develop pyelonephritis during pregnancy should be on prophylaxis with Nitrofurantoin or
Cephalaxin throughout the pregnancy.
 If patient with pyelonephritis does not improve in 48-72 hours, has persistently high fever order renal
ultrasound to rule out renal abscess.

Recurrent UTI: >3 infections/year


 Advise patient to urinate pre and post coitus
 Bactrim or Nitrofurantoin can be used daily

Asymptomatic Bateriuria: Positive urine culture in an asymptomatic patient.


 Treatment: No treatment unless
1: pregnant
2: Young children with vesicoureteral reflux
3: before urological procedure
4: After the removal of a bladder catheter that had been in place for less than one week

Patient with long term foley’s catheter:


 Asymptomatic bacteriuria: No treatment
 Symptomatic: Treat
Neutropenia:
 Mild: Absolute neutrophil count 1000-1500 cells/mm3
 Moderate: Absolute neutrophil count 500-1000 cells/mm3
 Severe: Absolute neutrophil count <500 cells/mm3
 When neutropenia is secondary to chemotherapy use Granulocyte-colony stimulating factor (Filgrastim)
or Granulocyte macrophage-colony stimulating factor (Sargramostim)
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Febrile Neutropenic Patient:


 Use antibiotic empirically, which covers Pseudomonas
 Ceftazidime or Cefepime or Imipenem (As monotherapy)
 Antipseudomonal penicillin+Aminoglycoside
 Ceftazidime or Cefepime + Aminoglycoside
 If patient has hypotension, Mucositis, skin or catheter site infection- Vancomycin+Ceftazidime
 If patient continue to be febrile after 5 days Add antifungal therapy (Amphotericin B, lot of centers
use Voriconazole or Caspofungin these days as they are better tolerated)
Meningococcemia
 Fever, stiff neck, headache with +ve Kernig’s sign (signs and symptoms of meningitis) + Petechial rash.
 Treatment: Penicillin G Intravenous is Drug of choice, ceftriaxone, cefotaxime. If allergic to penicillin,
use Chloramphenicol (s/e-Bone marrow suppression)
 Prevention: Droplet Isolation for 24 hour after starting therapy
 Meningococcal infection is more common in patients with terminal complement deficiency (C5-C9)
 Meningococcemia patients suddenly developed hypotension, shock– most likely diagnosis adrenal
hemorrhage (Waterhouse Friderichsen syndrome) T/t: IV Corticosteroid + treat meningococcal
infection.

Meningococcal Prophylaxis
 Population exposed who need prophylaxis: House hold contact, Day care center contact, coworker in the
same office, exposure to oral and respiratory secretion (Intimate kissing, mouth-to-mouth resuscitation,
endotracheal intubation or endotracheal tube management like suction)
 Population exposed does not need prophylaxis: School and work contact (Unless work in the same office),
hospital contact
 Drugs used for prophylaxis:
Rifampin 600mg BID x 2 days
Ciprofloxacin- 500mg PO x 1 dose
Ceftriaxone- 250mg IM x 1dose.

Whooping Cough
 Caused by Bordetella pertussis
 Young child with fever, cough which is paroxysmal and end with a high pitched inspiratory whoop with
lymphocytosis (80% lymphocytes)
 Treatment: Erythromycin
 Prevention: Infant and susceptible adults with significant exposure should receive prophylaxis with
Erythromycin for 10 days
 Note: 5% of infants getting Erythromycin can develop Infantile hypertrophic pyloric stenosis

Cat Scratch Disease


 Caused by Bartonella Henselae
 Usually in patients who work with animals (Veterinarian) comes with fever, malaise, tender regional
lymphadenopathy, occasionally h/o scratch by cat is there.
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 Confirmed by aspiration or biopsy of lymph node
 In children one of the causes of fever of unknown origin and usually associated with hepatosplenomegaly.
 Treatment: Adult: Azithromycin
Children: Rifampin + Azithromycin
Rat Bite Fever
 Cause: Streptobacillus moniliformis, spirillum minor
 Fever relapsing or intermittent, rash, asymmetrical polyarthritis and history of rat bite or patient is from
rat-infested slum dwelling.
 T/t: Penicillin G, if allergic Tetracycline.

Vibrio Vulnificus Infection


 Injury in sea water or after cleaning fish patient develops cellulitis with hemorrhagic bullae and necrosis.
 History could be hand injury while opening oyster or leg injury while launching boats.
 Treatment: Doxycycline

Complement deficiency
 C1, C2, C4 def: Recurrent Infection with encapsulated bacteria (Strep, H. Influenzae)
 C5-9 def: Recurrent meningococcal and gonococcal infection
 Best single test to screen complement def CH50

Reye’s Syndrome
 Rapidly progressive hepatic failure and encephalopathy (↑AST/ ALT/PT/Bilirubin/Ammonia level)
 Cause: Aspirin in patients with influenza or varicella
Drug-induced fever:
 Usually after days to weeks, but can occur after several years
 Can have associated rash
 Mostly associated with increased liver enzymes
 Common drugs are: Antimicrobials (sulfonamides, penicillins, nitrofurantoin, vancomycin,
antimalarials), H1 and H2 blocking antihistamines, Antiepileptic drugs (barbiturates and phenytoin),
Iodides, Nonsteroidal antiinflammatory drugs (including salicylates), Antihypertensive drugs
(hydralazine, methyldopa) Antiarrhythmic drugs (quinidine, procainamide) Antithyroid drugs
Brucellosis
 After exposure to animals or animal products, especially consumption of unpasteurized goat milk
cheese.
 It is important to remember that pasteurization is not required for certification of imported cheeses, so
consumption of imported cheeses could lead to the infection.
 Clinical features: Fever, arthralgia, hepatosplenomegaly
 Investigation: serum agglutinin, or Brucella antibody, Blood culture
 Treatment:
 Children: Oral trimethoprim-sulfamethoxazole plus rifampin for six weeks.
 Adult: Doxycycline combined with streptomycin or rifampin for six weeks.
Tularemia
 Caused by Francisella sp.
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N. D. Agrawal, MD
 H/o animal handling (Rabbit, Cat scratch) or tick or insect bite (Horseflies, Deerflies)
 Clinical feature: fever and a single erythematous papuloulcerative lesion with a central eschar and tender
regional lymphadenopathy.
 Inv: Antibody, Francisella tularensis or ELISA.
 Histologic examination of lymph nodes may be similar to cat scratch disease
 Treatment: Streptomycin is drug of choice.

Leptospirosis
• Caused by Spirochete, Leptospira interrogans.
• Typically after exposure to the environment contaminated by animal urine.
• Risk factors for infection include :
• Occupational exposure — farmers, ranchers, veterinarians, sewer workers, rice field workers, military
personnel
• Recreational activities — fresh water swimming, canoeing
• Household exposure — pet dogs, infestation by infected rodents.
• In the United States, Hawaii consistently reports the most cases of any state
• Clinical feature: fever, rigor with conjunctival suffusion.
• Weil's syndrome is the most severe form of leptospirosis and patients with this syndrome presents with
jaundice, hepatic and renal failure.
• Elevated creatine kinase is another useful clue for the diagnosis.
• Blood and CSF cultures are positive during the first 10 days of the illness. Urine cultures become
positive during the second week of the illness and up to 30 days after the resolution of symptoms.
• Serological tests are ELISA, microscopic agglutination test (MAT)
• Treatment:
• Mild Disease: Adults; Doxycycline Children: amoxicillin
• Severe Disease: I.V. Penicillin, Ceftriaxone, or cefotaxime
• PREVENTION — Vaccination available for domestic animals against Leptospirosis, but is not effective
in 100 percent of animals.

Trichinellosis
 Caused by Trichinella
 Suspect in patient with history of ingesting inadequately cooked meat, particularly pork and presenting
with periorbital edema, Muscle tenderness (myositis) and eosinophilia.
 Lab: Increased Creatinine kinase, LDH and eosinophils
 Serology: ELISA
 Muscle Biopsy is diagnostic but usually done if diagnosis is in doubt.
 Treatment: mebendazole or albendazole

Cysticercosis
• Caused by Taenia Solium (Pork tape worm)
• Mainly in Mexico, central and South America, Asia
• Prevalence is very high where pigs are raised
• Humans are incidental dead end host.

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N. D. Agrawal, MD
• Once eggs are ingested, embryos released in small intestine which penetrate the bowel wall and
disseminate hematogenously to other tissues and developed into Cysticerci, which are liquid filled
vesicles consisting of membranous wall and a nodule containing invaginated scolex.
• Mostly present with symptom of neurocysticercosis- seizure, headache
• Diagnosis: Confirmatory- brain biopsy
• MRI / CT can detect cyst but non specific
• ELISA
• Patient with symptoms (seizure, headache), MRI suggestive of neurocysticercosis, ELISA positive
start treatment and follow up with MRI for resolution of cyst.
• Treatment: 1: Albendazole + Prednisolone or Dexamethasone + Phenytoin or Carbamazepine for seizure
2: Praziquantel + Prednisolone or Dexamethasone + Phenytoin or Carbamazepine for seizure

Echinococcosis
• Caused by tapeworm mostly Echinococcus granulosus
• Latency period is very long, upto 50 years
• Mostly found in south and Central America, Middle East, China, western part of United States (Arizona,
New Mexico, California)
• Humans are infected accidentally, sheep are intermediate host and dogs are definitive host.
• Infection is high in areas, where sheep are raised.
• Pet dogs can be infected if eat home slaughtered sheep viscera
• Transmission to humans usually after eating vegetables or fresh produce contaminated with dog feces.
• Eggs swallowed carried to liver and forms Hydatid cyst.
• Cyst may be solitary or multilocular with daughter cyst
• Clinical Feature: Right upper quadrant pain, nausea, vomiting, may cause biliary obstruction and
produce obstructive jaundice, cholangitis. Liver cyst can rupture into peritoneum causing peritonitis and
occasionally severe anaphylaxis reaction
• Investigation: Ultrasound abdomen (Investigation of choice), If cyst present, confirm with ELISA or
indirect hemagglutination test
• Treatment: Surgery (main treatment) – If patient can tolerate it, especially if cyst > 10 cm.

• Medical Treatment:
• Albendazole (Better than Mebendazole)
• If large cyst and non surgical candidate / or refuses surgery  Albendazole + PAIR procedure {Cyst is
aspirated, then filled with protoscolicidal agent ( Hypertonic saline or ethanol) which will be aspirated
after 15 minute.

Strongyloidosis
 Caused by Strongyloides Stercoralis, mostly in warm climate, in south eastern states in USA.
 Larvae penetrate the skin, migrate to lung via blood  ascend the tracheobronchial tree and swallowed
 mature to adult worm in the mucosa of duodenum and jejunum and live there. Female worm
produces eggs which are excreted in the feces.
 Infection due to contact with soil contaminated with human feces

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N. D. Agrawal, MD

 Clinical Features; Serpiginous skin lesion on feet, buttocks, GI symptoms (upper abdominal pain,
nausea, vomiting diarrhea), Pulmonary symptoms (dry cough, dyspnea, wheezing, hemoptysis) with
eosinophilia
 Investigation: Larva in stool or duodenal aspirate
ELISA
 Treatment: Thiobendazole, if can not tolerate, Ivermectin

Cutaneous Larva Migrans


 Secondary to penetration of skin from infective larva of animal hookworms (usually Ancylostoma
Brazilience) which migrates into superficial tissue and produce the characteristic serpiginous eruption
 Usually after contact with soil, sand or other material contaminated with feces of dogs or cats mostly
found in warmer climate south eastern part of United States (History of visit or play in sandy beach or
sand box)
 Rash is usually on feet, buttock and abdomen
 Diagnosis: Clinical
 Treatment: Ivermectin or Albendazole oral

Chagas’ Disease
 Trypanosoma Cruzi infecting heart, esophagus and colon.
 Transmitted by Reduviid Bug or animal reservoirs (Raccoons, Armadillos etc)
 History of travel to Central or South America or emigrated from there.
 Most common presenting symptom: dysphagia (secondary to Achalasia), Constipation (secondary to
megacolon), CHF (Secondary to cardiomyopathy)
 Labs: hemagglutination test for Trypanosoma
 T/t: Nifurtimox and Benznidazole

Dengue Fever
 Caused by Dengue virus, after mosquito bite
 Mostly within 14 days of travel
 Most cases have been identified after travel to Puerto Rico, U.S Virgin Island or abroad (Mexico, South
East Asia, Africa and Middle east)
 Fever, headache, severe muscle and joint pain, eye pain (called Break bone fever) associated with
leucopenia, thrombocytopenia and elevated AST (serum aspartate transaminase)
 No specific treatment
Bioterrorism

Small Pox: vesiculo pustular rash, all in one stage (to differentiate from chicken pox)
Vaccination: available for
 1:Army
 2: Health care workers
 3: 1st emergency responders
 S/E of vaccine Encephalitis, Blindness
 Treatment: Cidofovir
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 Post-exposure prophylaxis: Vaccinate with in 3 days of exposure.

Anthrax
 Cutaneous Anthrax- ulcerative lesion with surrounding erythema and induration, no pain
 Inhalational anthrax- fever, dyspnea, pleural effusion, widening of mediastinum, hemorrhagic
mediastinits
 Prophylaxis: Ciprofloxacin, Levofloxacin, Doxy
 Treatment: same as above.

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