case 11. a baby is born with a rash identical to that...

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Case 11. A baby is born with a rash identical to that seen in the baby. Questioning reveals that the mother had a febrile illness during the second trimester of pregnancy. Examination reveals diffuse raised purple skin lesions. There is no pallor, jaundice, or cyanosis. The eyes are normal externally, the heart has a 3/6 systolic murmur, and there is enlargement of both the liver and the spleen. There is no LAP. ١

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Page 1: Case 11. A baby is born with a rash identical to that …iacld.ir/DL/modavan/viruses/casestudydrsobooti.pdfCase 11. A baby is born with a rash identical to that seen in the baby. Questioning

Case 11. A baby is born with a rash identical to that seen in

the baby. Questioning reveals that the mother had a febrile

illness during the second trimester of pregnancy. Examination

reveals diffuse raised purple skin lesions.

There is no pallor, jaundice, or cyanosis. The eyes are normal

externally, the heart has a 3/6 systolic murmur, and there is

enlargement of both the liver and the spleen. There is no LAP.

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What is your differential diagnosis?What would you like to know?

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Page 3: Case 11. A baby is born with a rash identical to that …iacld.ir/DL/modavan/viruses/casestudydrsobooti.pdfCase 11. A baby is born with a rash identical to that seen in the baby. Questioning

CHEAP TORCHES:CHEAP TORCHES:C: ChickenpoxH: Hepatitis B/C/EE E t iE: EnterovirusA: AIDS (HIV)P: Parvovirus B19T: ToxoplasmosisO: other (GBS, Listeria, Candida,T.B, LCMV)R: RubellaR: RubellaC: CMVH: HSVE E thi l STD ( h Chl di l HPV)E: Everything else STD (gonorrhea, Chlamydia, ureaplasma, HPV)S: Syphilis

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Page 4: Case 11. A baby is born with a rash identical to that …iacld.ir/DL/modavan/viruses/casestudydrsobooti.pdfCase 11. A baby is born with a rash identical to that seen in the baby. Questioning

In this case the rash was caused by rubella. The CRS may be associated with abnormalities affecting many organs: Ocular: cataract, microphthalmia, corneal opacityEar: deafnessH t CHDHeart: CHDBrain:MicrocephalyLiver: HepatitisLiver: HepatitisB.M: Anemia/ ThrombocytopeniaBone: Linear Lucencies in long bones (“celery stalk”appearance)

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The usual methods used to diagnose intrauterine infectionThe usual methods used to diagnose intrauterine infection

infection MethodRubella serologyCMV PCR on blood, urine viral cultureHIV DNA PCRLCMV SerologyS philis serolog (PCR)Syphilis serology(PCR)Toxo Serology

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Page 6: Case 11. A baby is born with a rash identical to that …iacld.ir/DL/modavan/viruses/casestudydrsobooti.pdfCase 11. A baby is born with a rash identical to that seen in the baby. Questioning

CASE 12. A 6 y/0 girl complains of weakness and muscle pain and

tightness in her thighs and legs. About 1WK earlier she had a fever,

sore throat, and cough. On examination she can’t stand nor walk due

to weakness. Her thighs and calves are tender. Sensation and DTR

are NL. Examination of the back and upper limbs is N.L.

What might be wrong with her?

What would you like to know?

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The DDX is one of generalized weakness but preserved higher

function. This suggests a lower motor neuron lesion affecting her

lower limbs. The possible levels of disease should be considered

anatomically. It is useful to consider possible etiologies of disease

for each of these sites. The DDX should include the infectious and

noninfectious disease.

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Causes of acute flaccid weakness :Causes of acute flaccid weakness :

(A) Spinal cord : spinal shock/ transverse myelitis(A) Spinal cord : spinal shock/ transverse myelitis

(B) Ant. Horn cell: polio/ other enterovirus/ WNV(C) Peripheral nerve: GBS/ Diphtheria/ toxins/ Acute intermittent porphyria(C) Peripheral nerve: GBS/ Diphtheria/ toxins/ Acute intermittent porphyria

(D) Neuromuscular junction: botulism/ snake bites 

(E) Muscle: myositis/ electrolyte disturbance (E) Muscle: myositis/ electrolyte disturbance 

(F) Pseudo paresis (localized) : skeletal disease/ trauma/ osteomyelitis/ septic arthritis/ congenital syphilis 

(G) Unknown mechanism: tick paralysis

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Th   i   d  l   d  i   hi   i  i di   l  The pain and muscle tenderness in this patient indicate muscle inflammation (myositis) as the cause of the weakness.

Acute muscle disease may be due to injury, inflammation (myositis), or a b li  di d  f   l  h   k  A   i i i   ll  metabolic disorder, for example, heat stroke. Acute myositis is usually 

caused by a viral infection such as influenza, enterovirus, HIV. This is referred to as benign acute childhood myositis, which is to be distinguished from the myositis accuring with dermatomyositis or distinguished from the myositis accuring with dermatomyositis or polymyositis, which have a prolonged  course and can result in significant long‐term disability. Patient with benign acute myositispresent with acute onset of weakness and muscle pain and tenderness, present with acute onset of weakness and muscle pain and tenderness, must frequently affecting the calf muscles. The muscles may be swollen and the weakness may be profound. The dangers of myositis are respiratory failure and rhabdomyolysis.p y y y

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The diagnosis of myositis can be confirmed by the demonstration of The diagnosis of myositis can be confirmed by the demonstration of 

elevated CPK activity in the serum. Myoglobinuria manifests as red, 

clear urine (like rose wine) as opposed to red  cloudy urine that clear urine (like rose wine) as opposed to red, cloudy urine that 

occurs with hematuria. In this circumstance a urine dipstick test 

that is positive for blood in the absence red cells on microscopy is that is positive for blood in the absence red cells on microscopy is 

highly suggestive of myoglobinuria. A microbiological diagnosis of 

the cause of myositis is not usually helpful, unless HIV infection is y y p

suspected. Treatment is primarily supportive, entailing analgesia 

and a very high fluid intake. If myoglobinuria is present the urine 

should be alkalinized to prevent injury to the renal tubules. 

Monitoring of respiratory function is essential. 

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Case 13. A 6 month – old boy presents with watery diarrhea and a tem. : 38.5 ْ◌ /c

Wh t i  th   t i t t  t  f th   li i l  l ti ? What is the most important aspect of the clinical evaluation? 

What is the likely clinical diagnosis, and what are its possible causes?

What do you want to do?

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The most important question addresses the physiologic diagnosis, namely: what is his hydration status? The sign of dehydration are: 

Decreased urine output Decreased urine output Sticky oral mucosa Decreased skin turgorS k    Sunken eyes Tachycardia Poor peripheral perfusion and L.O.C. (shock) 

what is the likely diagnosis? This is most likely a case of acute infectious diarrhea (acute GE). The possible causes are listed in next slide. 

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Causes of acute infectious diarrhea 

Virus: Rota  Adeno  Noro  Astro  Virus: Rota, Adeno., Noro., Astro. 

Bacteria: salmonella, shigella, campylobacter, E. coli, yersinia, vibrio cholera  vibrio parahaemolyticus  clostridium difficile  vibrio cholera, vibrio parahaemolyticus, clostridium difficile, clostridium perfringens

Parasites: giardia  C  Parvum  cyclospora  I  belli  E  Histolytica  B  Parasites: giardia, C. Parvum, cyclospora, I. belli, E. Histolytica, B. coli

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lComplications: 

1. Dehydration y

2. Metabolic and electrolyte disturbances 

3. Bacteremia

4. HUS 

5. Toxic encephalopathy 

6. Chronic diarrhea 

7. Colonic perforation 

8. Reactive arthritis 

9. GBS

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Causes of altered mental status in children who have or have had diarrhea  Shock from dehydration Shock from dehydration Metabolic and electrolyte disturbance 

Hypoglycemia H l i  Hyperglycemia HyponatremiaHypernatremia

VascularStroke HUS

Iatrogenic (rapid correction of hypo/ hyper natremia)Complication of bacteremia (meningitis)shigellosisshigellosis

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Differential diagnosis of intestinal symptoms and signs Vomiting, no diarrhea 

Gastritis Food poisoning Raised ICP Intestinal obstruction (intussusception)Parental infection

Hematochezia, no diarrheaMeckel’s diverticulumIntussusceptionPolypProfound upper intestinal bleeding

Bloody diarrheaMilk protein allergy IBD

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Epidemiological, clinical, and stool features associated with different Epidemiological, clinical, and stool features associated with different enteric infection, and tests used for their confirmation

Microorganism  epidemiology  clinical stool  testMicroorganism  epidemiology  clinical stool  testRotavirus  winter  acute  no blood  Ag Adenovirus  ___ acute  no blood  tissue cultureNorovirus outbreak  acute, vomiting  no blood  RT‐ PCRSalmonella  animals, eggs, meat acute, fever  ± blood, PUS culture Shigella day care, human  acute, fever  ± blood, PUS    culture Campylobacter  poultry   acute  ± blood, PUS    culture 

i i k  bl d l  yersinia pork  acute ± blood culture Giardia daycare, water   acute, chronic  no blood  micro./ Agcryptosporidium  water, outbreak  acute, chronic  no blood  micro./ AgCyclospora outbreak  acute  chronic  no blood  microCyclospora outbreak  acute, chronic  no blood  microE. Histolytica travel  acute, chronic  blood  micro. /Ag

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A ti i bi l th   f  t i  i f ti  Antimicrobial therapy of enteric infections 

Microorganism  antimicrobial agents Salmonella  none  unless bacteremia suspected Salmonella  none, unless bacteremia suspected 

ceftriaxone, TMP/SShigella ampicillin, TMP/S, ceftriaxone

azithromycin, fluoroquinoloneC l b  j j i i h i  fl i lCampylobacter jejuni azithromycin, fluoroquinolone

gentamicin, imipenemYersinia enterocolitica none, unless bacteremia suspected 

ceftriaxone, TMP/S, gentamicince t a o e, /S, ge ta cE. Coli  TMP/S, Flouroquinolone, rifaximinC. Difficile metronidazole, oral vancomycinGiardia metronidazole, nitazoxanideC  P it idC. Parvum nitazoxanideCyclospora TMP/SI. Belli  TMP/SE. Histolytica metronidazole, tinidazoley

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Case 14. A premature infant in the NICU being ventilated for HMD is noted to have temperature instability, dark red spots on the skin, and a swollen red ankle. Further examination reveals a 3/6 ejection systolic heart murmur, heard loudest at the upper sternal border. She has a venous and arterial vascular catheter in place  The abdominal venous and arterial vascular catheter in place. The abdominal examination is NL. 

What is the differential diagnosis? 

What would you do? What would you do? 

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Dark red spots on the skin suggest the possibility of hemorrhage or p gg p y ginfarctions of the skin. The red, swollen ankle suggests a septic arthritis or osteomyelitis. Tem. Instability suggests a systemic infection. A unifying diagnosis would be a systemic (bloodstream) bacterial or unifying diagnosis would be a systemic (bloodstream) bacterial or fungal infection associated with skeletal infection, and causing (a) a hemorrhagic tendency through the mechanisms of thrombocytopenia or DIC or (b) emboli due to IE. Nosocomial infection is important. The potential routes of infection are through: 

Vascular access sites Vascular access sites 

Lungs (intubation)

Intestine

U.T.I

*** Staph./ enterococci/ candida/ gram‐neg. bacilli 

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Specific clinical evaluation 

Examination of the optic fundi

Examination of all vascular access sites 

U/A 

B/C , CBC 

Aspiration of ankle / skin lesions (gram stain/ culture) 

Echo. 

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Antimicrobial treatment 

(a) Gram positive cocci (staph.): vancomycin+nafcillin+gentamicin. The reason for using both vancomycin and nafcillin is that for susceptible organisms, nafcillin is superior to vancomycin. However, the g , p y ,vancomycin is necessary in case the organism is resistant to β‐lactamAB (MRSA). Gentamicin accelerates the clearance of the staph. from the blood. 

(b) Gram negative rods (enteric bacilli or p. aeruginosa): ceftazidime + amikacin/ gentamicin

(c) Yeasts: amphotericin B (in less severly ill patients with intravascular –(c) Yeasts: amphotericin B (in less severly ill patients with intravascular line – associated fungemia, and without endocarditis, and in whom the vascular line can be removed, fluconazole would be appropriate. 

(d) If the gram stain does not reveal an ogranism  initial treatment (d) If the gram stain does not reveal an ogranism, initial treatment should be directed at staph. and gram negative rods with vancomycin, nafcillin, gentamicin, or amikacin and a 3rd – generation cephalosporin  cephalosporin. 

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The gram stain from a skin aspirate of this patient shows gram positive 

i i   l   h   i l    f  h l i   h   ki  cocci in clusters, the typical appearance of staphylococci. The skin, 

B/C, ankle joint fluid grew out staph. aureus susceptible to methicillin. 

Further evaluation revealed an aortic vegetation  providing additional Further evaluation revealed an aortic vegetation, providing additional 

evidence of IE. She was treated successfully with nafcillin. 

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CASE 15. A 3 Y/O boy who broke out with chickenpox 5 days ago seems to be getting worse after initial improvement. He has a high fever, his skin 

is red all over  and he seems a little confused  is red all over, and he seems a little confused. 

Wh t  i ht b  th   bl ? What might be the problem? 

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The most likely problem is that this boy has developed a complication of y p y p pchikenpox. The most common complication is secondary bacterial infection of skin lesions with s. pyogenes or S. aureus. The child’s 

illness is characterized by fever, confusion, and diffuse erythroderma. Given the apparent severity of the child’s condition and the 

combination of clinical abnormalities, he probably has streptococcal/ combination of clinical abnormalities, he probably has streptococcal/ staphylococcal TSS.

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Further clinical evaluation should be directed at determining the adequacy of his perfusion and at finding a septic focus that might be drained. This is very important in TSS. Management should entail the drained. This is very important in TSS. Management should entail the following: 

(a) Ensuring adequate perfusion with IV fluid and vasopressors, if necessary.

(b) Draining any focus of pus and sending specimens for gram stain and culture; a B/C should also be performed culture; a B/C should also be performed 

(c) Antimicrobial therapy: vancomycin (MRSA) + oxacillin/ nafcillin/ cephazolin (strep. Pyogenes/ MSSA) + Clindamycin (halt toxin p ( p y g ) y (production)

(d) I.V.I.G

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