12/8/2021 Final Infectious

Dox
These are all possible cases taking from
various files and combined.
CASE 1
A 40-year-old woman presents to her physician with an erythematous annular
patch with central clearing on her left forearm. The patient states that the rash
began as a small red papule about 5 days ago and has grown progressively
larger. She also complains of fatigue, headache, myalgias, and intermittent
arthralgias. She has remained afebrile, and her vital signs are stable. Physical
examination is significant for 8×7-cm erythematous patch on her left forearm
that has concentric rings of redness and a clearing center. She also has cervical
and axillary lymphadenopathy. The remainder of the examination is
unremarkable. She has been on a hiking trip with her family 10 days ago but
nobody else developed any symptoms. She recalls no sick contacts.

What is the most likely diagnosis? How did this patient get infected? • Lyme
disease, a multisystem inflammatory disease caused by borrelia
burgdorferi, must be considered in a patient with the history of hiking and
a classic “bull’s-eye” rash of erythema migrans in combination with
constitutional symptoms.
• Ixodes scapularies tick (deer tick) is the vector of this spirochete

How can this condition be diagnosed?

The diagnosis of Lyme disease is clinical and is confirmed by serologic testing in
later disease. (Sensitivity of serologic testing is approximately 50% in early
disease and increases to over 90% by the later stages). The fact that the
patient has gone hiking, and the history that the rash expanded over several
days and surpassed 5 cm in diameter, are useful clues. Diagnosis is aided by
serologic testing in later disease, which should include antibody testing by
enzyme-linked immunosorbent assay (ELISA). If positive, follow-up with
Western blot testing.

The patient’s husband presents to the physician 6 months later complaining

of bilateral facial palsy. What is the most likely diagnosis?
This patient has Bell’s palsy, most likely caused by disseminated B. burgdorferi.
Presentation of disseminated disease can occur days to months after the tick
bite. CNS involvement can include meningitis and cranial nerve palsies .

What other symptoms could this female patient expect to develop over time
if the condition is not treated?
Lyme disease can be divided in stages:
• Stage 1 – early localized infection: Erythema migrans
• Stage 2 – early disseminated infection: Migratory musculoskeletal pain
and migratory arthralgias accompanied by malaise and fatigue are the
most common, less likely (14 % of patients): neurologic manifestations
 encephalopathy, neurocognitive dysfunction, peripheral neuropathy (VII
CN palsy) and nonspecific symptoms (headache, fatigue) also occur.
Even less commonly (8%) – Cardiac involvement - carditis, fluctuating AV
block of any type; LV dysfunction, cardiomegaly
• Stage 3 – Late persistent infection: 60 % - develop arthritis: oligoarticular
in large joints, chronic neurologic involvement, Acrodermatitis Chronical
artophicans,

What is the most appropriate treatment for this condition? • Early Lyme
disease – doxycycline (amoxicillin, cefuroxime, erythromycin - alternatives)
for children <9 years –– amoxicillin
• Neurologic involvement, 3rddegree AV cardiac block – IV ceftriaxone
 CASE 2
A 22-year-old college student is your patient in the emergency room. When
you walk into the room, he is lying on the examination table, with his arm
covering his eyes. You look at his chart and see that his temperature is39°C
(102.3°F), heart rate 110 bpm, and blood pressure 120/80 mm Hg. When you
ask how he has been feeling, he says that for the past 3 days he has had fever,
body aches, and a progressively worsening headache. The light hurts his eyes
and he is nauseated. He has vomited once. He reports no diarrhea, cough, or
nasal congestion. On examination, he has petechial skin rash on his trunk. His
pupils are reactive to light, but he feels severe discomfort when you shine the
light into his eyes and begs you to stop. Ears and oropharynx are normal.
Heart, lung, and abdomen examinations are normal. Neurologic examination
reveals no focal neurologic deficits, but passive flexion of his neck worsens his
headache, and he is unable to touch his chin to his chest. According to him,
one other student in his dormitory has recently been hospitalized, but he
doesn’t know why.

1. What condition are you concerned about? Bacterial meningitis 2. What

bacterial organisms are the most common causes of this disease? Strep.
Pneumonia, N. meningitides; L. monocytogenes – in very young or very
old; H. Influenza type B – no longer common in developed countries due to
vaccination
3. Based on the information given above, what organism is the most
likely cause of this patient’s condition? Neisseria Meningitides
(petechial rash)
4. What are the most likely symptoms of this disease?
Fever, nausea, vomiting, neck stiffness, photophobia, irritability, positive
Kernig and Brudzinski signs, decreased level of consciousness, seizures
and focal neurologic signs in severe cases, petechial or purpuric rash –
present in 80% of cases with N. meningitidis
5. What diagnostic test would confirm the suspected diagnosis? Lumbar
puncture
6. What are the classic findings seen on this test? turbid CS fluid,
Increased WBCs – Polymorphonuclear neutrophils; increased protein,
decreased glucose; Gram negative diplococcus
7. What is the appropriate treatment for this patient?
Treatment is begun empirically without waiting for the LP results: IV 3 rd
generation cephalosporin (ceftriaxone) + IV Vancomycin
dexamethasone is added to decrease the inflammation and reduce the
rate of neurologic complications) - in this particular patient this is the
best initial treatment
 In immunocompromised patients or very young and very old – IV
ampicillin – to cover Listeria monocytogenes
8. What is the prognosis of this condition? 10% of patients die despite
adequate therapy
9. What complications may follow this condition? Severe bacteremia and
DIC; Permanent skin scarring after purpuric skin lesions, amputation,
neurologic complications, hearing loss, temporary renal hypoperfusion.
Waterhouse-Friedrichsen syndrome – Hemorrhagic necrosis of one or
both adrenal glands – due to overwhelming meningococcemia – lead to
adrenal insufficiency and death
Hypervolemia, hypertension, and hemodilution (triple H)
CASE 3
You see a 25-year-old man in the clinic. You enter the room and see a healthy
appearing young man, who seems nervous. He finally admits that he has been
worried about a lesion on his penis. He denies pain or dysuria. He has no
previous history of sexually transmitted diseases (STDs) and has an otherwise
unremarkable medical history. He is afebrile, and his examination is notable
for a shallow clean ulcer on the shaft of his penis, which is nontender to
palpation. There are some nontender, inguinal lymph nodes bilaterally.

What is the most likely diagnosis? Syphilis

What is the cause of this disease? Treponema pallidum, a spirochete
What is the clinical course of this disease?
• PRIMARY SYPHILIS: Initial lesion of T pallidum infection, usually in the
form of a firm, nontender ulcer: the chancre(location: cervix,
rectom.labia, penis). ( cd4+ cd8+ , t lymp, macrophages)capillary
endothelial proliferation.
• SECONDARY SYPHILIS: Disseminated infection manifesting in a pruritic,
maculopapular diffuse rash that classically involves the palms and soles,
or the flat moist lesion of condyloma Lata. (WART) hyperkeratosis of
epidermis. Generalized non tender lymphadinopTY, abnormal liver
function test. Patchy alopecia, chondylomata lata- highly infectious
lesion.
• Latent syphilis - detected only by serological testing.
• TERTIARY (LATE) SYPHILIS: Symptomatic infection involving the central
nervous system( tabes dorsalis and peris), cardiovascular system- vasa
vasorum of aorta (ascending aortic aneurysm, or the skin and
subcutaneous tissues(gummas). Meningial syphilis( all meningial signs)

Is this infection transmitted trans placentally? YES - pregnant women with latent
syphillis may infect the fetus in utero.transmission can occur at any stage of
pregnancyfetal damage occurs at 4th month of gestation.

What are the characteristics of congenital form of this disease?

PULMONARY HEMORRHAGE, INFECTON, SEVERE HEPATITIS
( teatment before 16th week of preg prevents fetal damage.)

What diagnostic approaches are available for this infection? •

Nontreponemal tests: RPR and Venereal Disease Research Laboratory
(VDRL) tests, which actually are tests for antibodies against cardiolipin
lecithin-cholesterol complex that occur as part of the host reaction to T
pallidum - fairly sensitive for the detection of disease - they may be
nonspecific and may result in false-positive results.
 • Confirmatory testing in the form of specific antibody testing for T
pallidum - fluorescent treponemal antibody absorption (FTA-ABS) or
micro hemagglutination assay for Treponema pallidum (MHA-TP) test, is
the next step.
• Dark-field microscopy, in which scrapings from an ulcer are placed under
a phase contrast lens to actually identify the organisms, is the classic
method of diagnosis but is rarely performed today
• Screening: VDRL, RPR; confirmation: (FTA-ABS); assessment of response
to the therapy: RPR9rapid plasma reagin, VDRL veneral disease
research laboratory-CSF. Enzyme imunoassey test- EIA

What is the treatment of this condition?

Penicillin is the treatment of choice for syphilis
• Primary, secondary or early latent syphilis: 1 IM dose benzathine
penicillin; Penicillin allergic patients: Doxycycline, tetracycline • Late
latent, cardiovascular or benign tertiary (gummatous): benzathine
penicillin weekly for 3 weeks; Penicillin allergic patients: Doxycycline,
tetracycline or ceftriaxone;
• Neurosyphilis; Syphilis during pregnancy: penicillin; Penicillin allergic
patients – desensitize and give penicillin
Residual stigmata- saddle nose, centrally notched teeth, saber shin
 CASE 4
A 20-year-old male college student presents with abdominal pain, diarrhea,
and fever. He says that his symptoms started one day ago. He has had 10 stools in
the past day. He usually eats at home but reports having eaten chicken in the
college cafeteria three days ago. He has no history of gastrointestinal (GI) disease.
On examination he has a temperature of
37.8 C (100 F) and appears to be in pain. His abdomen has hyperactive
bowel sounds and is diffusely tender but without rigidity, rebound
tenderness, or guarding. A stool sample tests positive for blood and fecal
leukocytes. Stool cultures are sent and are subsequently positive for a
pathologic organism.

• What is the most likely diagnosis? Bacterial gastroenteritis • What is

the most likely pathologic organism? Campylobacter jejuni • List the 4
most common causes of similar presentation: 1. Campylobacter
jejuni
2. Salmonella
3. Shigella
4. E. coli in same sequence.
-c jejuni-Adapts for survival in GI mucosa layer- raw undercooked
meet(poltry),direct contact with infected animal,oral-anal sexual
contact,unpasturised milk.
Usually peaks during summer and autumn.
*c-fetus(extra intestinal disfunction)-subacute bacterial endocRDITIS.

What is the diagnostic approach this patient?

The differential diagnosis of acute gastroenteritis would include Salmonella,
Shigella, Yersinia, as well as Campylobacter.
Stools contain leukocytes, and/ or RBCs
Campylobacter often mimics ulcerative colitis and Crohn’s disease but is much
more common than either.
Definitive diagnosis would be made by culture of the stool and growth of
Campylobacter.
Additional symp: bloody dairrhea, hepatospleeno megaly, meningitis,
reactive arthritis, fever(unknown origin)

What is the Treatment of this condition?

Most often Campylobacter jejuni infection is self-limited and does not require
specific antimicrobial therapy.
Supportive care –electrolytes and hydration, is often the only treatment
needed.
If specific therapy is needed for severe disease, or infection in
immunocompromised patients, erythromycin, azithromycin,
alternative fluoroquinolones Antimotility agents – may prolong
symptoms What is the Prevention of this condition?
involves care in food preparation. Foods, especially chicken, should be
completely cooked, and exposure to raw or undercooked chicken or
unpasteurized milk should be limited, especially in pregnant or
immunocompromised persons
Complications: bacteremia, endocarditis,meningitis, HUS, guillain-
barre syndrome., reactive arthritis- cant see, cant pee, cant bend my
knee.

2 weeks later the patient wakes-up and is not able to move his feet. What is
this complication and what is the underlying pathophysiologic mechanism?
Why is this condition dangerous? What is the management of the patient?
Guillain-Barre syndrome – autoimmune demyelination of the peripheral
nerves – leads to ascending weakness/ paralysis of the muscles - may lead to
respiratory paralysis; management: intubation because it may lead to
respiratory failure., plasmapheresis or IV immunoglobulin; prognosis is
excellent
 CASE 5
A 26-year-old woman presents to the office with a 3-day duration of
discomfort with urination and increased urinary frequency. She has noted that
her urine has a strong odor as well. She denies abdominal pain, back pain,
vaginal discharge, or skin rash. She is diagnosed with uncomplicated cystitis.
What is the most common cause of this condition?
Extra-intestinal pathogenic E. coli (ExPEC)
Most likely mechanism of introduction of organism into the urinary tract:
Urethral contamination by colonic bacteria followed by ascension of the
infection into the bladder.

What are the most common symptoms and signs of this condition? Who is
under increased risk to develop urethritis/cystitis? - Females, pregnant
patients
Burning/discomfort with urination – dysuria; No fever. No costovertebral angle
tenderness. Abdominal exam – shows suprapubic tenderness.
What can cystitis complicate with? What is the most common presentation
of this condition?
PyelonephritTis - Burning/discomfort with urination – dysuria; presence of
fever. Costovertebral angle tenderness, or back pain, nausea/vomiting
uncomplicated cystitis, catheter associated UTIs.

What is the appropriate diagnostic approach to this patient? Diagnosis based

on Clinical presentation plus microscopic examination of urine sample - white
blood cells and numerous gram-negative bacteria.
What are the appropriate treatment options for uncomplicated mild UTI?
1. Nitrofurantoin – 5 days
2. TMP-SMX – 3 days
3. Fosfomycin – 1 dose
4. Ciprofloxacin, levofloxacin
Prevention- pregnant women- prenatal screening
CASE 6
A 33-year-old comes to your clinic for follow-up of recurrent upper abdominal
pain. He initially presented 3 weeks ago, complaining of an increase in
frequency and severity of burning epigastric pain, which he has experienced
occasionally for more than 2 years. Now the pain occurs three or four times
per week, usually when he has an empty stomach. The pain usually is relieved
within minutes by food or antacids, but then recurs in 2 to 3 hours. He admits
that stress at work had recently increased and that because of long working
hours, he is drinking more caffeine and eating a lot of take-out foods. His
medical history is otherwise unremarkable, and other than the antacids, he
takes no medications.

What is the most likely diagnosis? What bacteria can be associated with the
development of this condition?
Peptic ulcer – H. pylori
If the condition goes untreated, what conditions may develop?
1. Adenocarcinoma of the distal stomach
2. MALT lymphoma
3. Gastric carcinoma

What is the pathophysiologic mechanism of bacteria causing the disease?

Infiltration of mucosa by WBCs, inflammation-mediated damage of the
GASTRIC mucosa and reduction of somatostatin releasing D cells, that leads to
uninhibited production of gastrin, that increases HCL acid production, further
damaging the gastric mucosa. H pylori protects itself from acid by producing
the enzyme urease – neutralizes acid.

What are the diagnostic approaches to this patient?

Noninvasive tests: urease breath test, stool antigen testing, detection of
antibodies – stays positive for long time - cannot assess response to the
therapy
Invasive test: endoscopy and rapid urease testing of the biopsy sample;
or histopathologic exam of the sample taken Explain the mechanism of
urease breath test:
Patent drinks solution containing labeled urea (C 13), H. pylori metabolizes urea
with urease and releases water and C 13O2 - carbon is labeled, when the patent
exhales the CO2 – it contains labeled C13and we are able to detect it.

If this condition is found to be caused by bacteria, what are drugs used in

treatment?
• Triple therapy: Proton pump inhibitor (omeprazole, lansoprazole),
clarithromycin, amoxicillin (or metronidazole)
• Quadruple therapy: PPI, bismuth, tetracycline, metronidazole Wait for 1
month after finishing the therapy and perform the urease breath test to
assess the cure
 CASE 7
A 26-year-old woman is hospitalized with symptoms of fever, chills, malaise,
and joint discomfort in her hands and knees. She looks unwell, temperature
is 40.4°C, blood pressure 120/85 mm Hg, pulse 100/min. She is otherwise
healthy, with no significant medical history. She smokes cigarettes and
marijuana regularly, drinks several beers on weekends, and sometimes
injects heroin intravenously. Lungs are clear, abdomen is soft, and hand joints
are normal. Cardiac murmur is auscultated and heard best over the second
intercostal space on the left. On her forearms she has small nodules overlying
the superficial veins from injection drug use. She is diagnosed with Bacterial
endocarditis.

Which of the following is the most likely causative organism? Why?

Staphylococcus aureus(cogulase- fibrinogen to fibrin, catalase- h2o22 to h2o
and o2); risks - IV drug use, young healthy patient; involvement of the
tricuspid valve

Most commoncause of surgical wound infections

Pathophysiology- has protein a with prevents optimization and phagocytosis.

3 toxins: pyrogenic, exfoliate , cytotoxins.

TOXIC SHOCK SYNDROME: in healthy, young women- due to tampon.

Execissive immune activation which leads to multisystem damage .

What is the diagnostic approach to this patient?

Major Duke’s criteria:
• Positive Blood cultures
• Cardiac ultrasound- transthoracic, transesophageal – valvular
vegetations Minor Duke’s:
• Fever, predisposing lesion, risky behavior (IV drugs), embolic
phenomena, immunologic phenomena
Oslers node, roth spots.
A 34-year-old woman is at picnic, where she has a ham sandwich and potato
salad. Three hours after the meal, she feels nauseous and throws up. The
same bacteria causing the endocarditis in the previous patient is isolated
from the potato salad. How is it responsible for this woman’s symptoms? S.
aureus enterotoxin caused food poisoning. Toxin is heat stable. Symptoms
Start soon, is gone soon. Major symptom- vomiting, sometimes diarrhea.
Toxin stimulates vomitting centre of brain and peristaltic activity of intestines.
Treatment : supportive.
Another patient, a 17-year-old menstruating female develops multisystem
disease with hypotension, diffuse erythematous rash with desquamation of
skin on hands and feet. Same bacteria are responsible for her condition.
What is the pathophysiologic mechanism of the disease in this case? S.
Aureus releases toxic shock syndrome toxin1 (TSST-1) – accumulates in
tampons and acts as a superantigen and activates excessive immune response
– leads to multisystem damage.

Coagulase negative streptococcus: s.epidermus, s.saprophticus- biofilm device

surface- caused by devices

a 17-year-old menstruating female develops multisystem disease with

hypotension, diffuse erythematous rash with desquamation of skin on
hands and feet. Same bacteria are responsible for her condition. What is the
management of this patient?
Entirely supportive, reversal of hypotension, no antibiotics,

CASE 8
A 19-year-old woman presents for the evaluation of vaginal discharge that has
progressively increased over the past week. She is sexually active, has had four
lifetime partners, takes oral contraceptive pills, and occasionally uses
condoms. On examination, she appears in no acute distress and does not have
a fever. Her abdomen is soft with moderate lower abdominal tenderness. On
pelvic examination, she is noted to have a yellow cervical discharge and mild
cervical motion tenderness. No uterine masses. A Gram stain of the cervical
discharge reveals only multiple polymorphonuclear leukocytes.

What is the most likely diagnosis? Cervicitis / Pelvic inflammatory disease

What is the most likely cause of this symptom? Chlamydia trachomatis If
this condition goes untreated, what complication is likely, Fitzhugh Curtis
syndrome (perihepatitis)
infertility, ectopic pregnancy – ask why?
What can happen in population with HLAb27 genotype? – reactive arthritis –
can’t see, can’t pee can’t bend my knee .

What is the diagnostic approach to this patient?

Cervical discharge swabbing – no organism, increased WBCs, A direct DNA
probe test (NAAT)

What is the treatment of this patient? For uncomplicated infections

Tetracycline, doxycycline, erythromycin – 7 days; 1 dose of Azithromycin,
longer duration for PID or other complic. Cases.
What is the prevention of this condition? Condoms, screening of high-risk
groups

What other diseases can be caused by the same bacteria, but different
serotypes?
C. trachomatous serogroups A, B, C: trachoma, conjunctivitis C.
trachomatous serogroups D –K – STD– cervicitis, urethritis, PID C.
trachomatous serogroups L1, L2, L3 – lymphogranuloma venereum

CASE 9
7-year-old boy is brought to your office in January with the 2-day history of
fever, cough, and rhinorrhea. He complains of left ear pain since yesterday.
You diagnose him with acute bacterial otitis media .
1. What is the most likely bacterial cause of his symptoms? list 2
otherpathogens causing the similar presentation Streptococcus
 pneumoniae – most common, haemophilus Influenzas – nontypable
strains, Moraxella catharallis

2. What is the appropriate diagnostic approach to this patient? What

arethe characteristic findings on the physical exam? – otoscopy –
best initial test: red, swollen bulging tympanic membrane; Golden
test to find the
etiologic agent: - tympanocentesis (too invasive, almost never done)

3. List the other conditions most likely caused by the same pathogen;S.
pneumonia is the most common cause of: pneumonia, sinusitis,
otitis media, one of the most common cause of meningitis;
4. What is the most appropriate Treatment of this patient’s condition?
Empiric antibiotics that cover all most common causes: amoxicillin+
clavulanic acid – the best initial
5. Who has increased risk to develop diseases caused by
thismicroorganism and why?
Repeated pneumococcal infections: it’s an encapsulated bacterium,
removal of that kind of bacteria is facilitated by spleen; so, a splenic
patient - higher risk of encapsulated organism infection

CASE 10
A 28-year-old female presents to your office. You diagnose her with post
infectious glomerulonephritis. Three weeks ago, she had impetigo on her
forearm, which resolved without treatment.

IMPTIGO- superficial skin infection due to lack of hygene

Erysyphillis- infection of skin only, superficial

 1. Describe the most likely presenting symptoms of post-
infectiousglomerulonephritis;
Hypertension, hematuria, oliguria, edema, sometimes fever, nausea,
anorexia, headache)
2. What organism is the most likely because of her renal disease?
Streptococcus pyogenes - GAS
3. What is the underlying pathophysiologic mechanism of her currentillness? –
type 3 hypersensitivity = circulating antigen-antibody
complexes accumulate in glomeruli and initiate the infection
4. List the other medical conditions caused by the same organism; sponges –
pharyngitis, impetigo, scarlet fever, erysipelas, cellulitis, necrotizing fasciitis,
toxic shock syndrome; rheumatic fever;
5. What could have prevented development of this condition? – nothing

CASE 11
A 9-year-old patient develops sore throat. He has fever 38.2oC. On physical
exam, Pharynx is erythematous with purulent exudates covering posterior wall.
2 small pustules are visualized on tonsils. Patient has tender cervical
lymphadenopathy.

1. What organism is the most likely cause of this patient’s illness?

Streptococcus pyogenes – GAS - s. pharyngitis
 2. What is the appropriate diagnostic approach?
Clinical findings, rapid strep testing, Throat culture – golden standard

3. What is the serious complication of this infection if it is left untreated?

What is the prevention? Describe the pathophysiology of this
condition – Rheumatic fever –type 2 hypersensitivity - antibodies
mistakenly attack the host tissues due to antigenic mimicry
4. Talk about major and minor Jones criteria- Major: migratory polyarthritis,
carditis – may lead to mitral stenosis most commonly, subcutaneous
nodules, erythema marginatum, Sydenham’s chorea; minor: fever, ESR,
CRP – elevated; Leukocytosis, prolonged PR on ECG, previous episode of
RF

5. What is the possible renal complication of this patient’s condition?

Describe the pathophysiology of this condition: post streptococcal
Glomerulonephritis – Type 3 hypersensitivity. – antigen-antibody
complexes circulate and get accumulated in the glomerulus – initiate
inflammation.

CASE 12
A 5-year-old child is taken to pediatrician because of severe sore throat and
fever of 4 days’ duration. Today the patient abruptly developed a skin rash.
You diagnose him with scarlet fever.

1. What is the most likely cause of this illness? Streptococcus pyogenes –

GAS,
a. what causes skin rash? Erythrogenic toxins A, B, C
2. Describe the characteristic clinical findings on the physical
exam;pharyngeal injection, swollen bright-red tonsils and tongue with
discrete white exudates; enlarged tender anterior cervical lymph nodes.
Examination of the skin reveals a diffuse erythematous rash – slightly
 rough, sand-paper texture. Pastia’s lines - The rash intensifies on the
neck, chest folds of axilla and groin (flexor surfaces) , strawberry tongue.
3. What is the management of this condition? Penicillin or erythromycin

4. What is the possible serious complication of this infection if it is

leftuntreated? Describe the pathophysiology of this complication;
Rheumatic fever – type 2 hypersensitivity - antibodies mistakenly attack
the host tissues due to antigenic mimicry; previous episode of RF
5. Talk about major and minor Jones criteria Major and minor Jones
criteria - Major: migratory polyarthritis, carditis – may lead to mitral
stenosis most commonly, subcutaneous nodules, erythema marginatum,
Sydenham’s chorea; minor: fever, ESR, CRP – elevated; Leukocytosis,
prolonged PR on ECG,

CASE 13
5-year-old girl is brought to the emergency room by the worried parents. The
girl has been irritable for the past 4 days. Today morning, she complained of
sore throat and refused to swallow the food during the day. On admission, she
refuses to lie down supine to be examined and is bending forward with the
neck extended. She has fever of 39.7oC and is drooling. Respiratory rate is 40
with shallow breaths and use of accessory respiratory muscles. Pharynx is
erythematous. Her lungs are clear.
1. Based on this clinical presentation, what is your primary diagnosis?
Whatis the most likely causing organism?
Hemophilus influenza type B - epiglottitis
2. What could have prevented development of this condition? vaccination
3. What is the best next step in the management of this child? – keep
the airway patent - intubate
 4. What is the treatment of this condition? – intubation and cephalosporin
- ceftriaxone
5. While managing this child, what other infectious causes should
beincluded in your differential diagnosis? – strep pharyngitis, diphtheria

CASE 14
A 16-month-old child is brought to the emergency room following a seizure. His
mother says that he had a cold for 2 or 3 days with a cough, congestion, and
low-grade fever, but today he became much worse. He has been fussy and
irritable. He then had two grand-mal seizures. His mother reports that he has
not received all of his immunizations. On examination his temperature is
38.1°C (100.5°F), his pulse is 110 beats per minute, and he appears very ill. He
grimaces when you try to bend his neck. His skin is without rash and his
HEENT
(head, eyes, ear, nose, throat), cardiovascular, lung, and abdominal
examinations are normal. His white blood cell count is elevated, and a CT scan
of his head is normal. You perform a lumbar puncture, which reveals
numerous small gram-negative coccobacilli.
1. What organism is the most likely etiology of this illness?Hemophilus
influenza type B - invasion from nasopharynx-all parts( meninges,
bones,joints)
2. What could have prevented development of this condition?vaccination
 3. What other clinical presentations can be caused by the same
pathogen?
Epiglottitis- dysphagia,chocking,tumbprint sign on xray, cellulitis- bluish red colour
skin, less common- osteo myelitis, septic arthritis, renal disfunctions.
4. What is the treatment of this condition? –
Cephalosporins, glucocorticoids,ceftriaxone - epiglottitis.
5. Non-encapsulated form of this bacteria can also cause human
diseases.
List several of those; otitis media, sinusitis,
exacerbations in COPD patients

CASE 15
A 14-day-old infant is brought to the pediatric emergency room by her
panicked mother. The child has developed a fever and has been crying nonstop
for the past 4 hours. She has fed only once today and vomited all of the
ingested formula. The baby was born by vaginal delivery after an
uncomplicated, full-term pregnancy to a healthy 22-year-old gravida1 para1
(one pregnancy, one delivery) woman. The mother has no history of any
infectious diseases and tested negative for group B Streptococcus prior to
delivery. The baby had a routine check-up in the pediatrician’s office 3 days
ago, and no problems were identified. On examination, the child has a
temperature of 38.3°C (100.9°F), pulse of 140 beats per minute, and
respiratory rate of 32 breaths per minute. She has poor muscle tone. Her
anterior fontanelle is bulging. Her mucous membranes are moist, and her skin
is without rash. Her heart is tachycardic but regular, and her lungs are clear.
Her white blood count is elevated, a urinalysis is normal, and a chest x-ray is
clear. A Gram stain of her cerebrospinal fluid (CSF) from a lumbar puncture
shows gram-positive coccobacilli.
What is the most likely diagnosis? Meningitis

What organism is responsible for this infection? Listeria monocytogenes , trnsmission

thruogh food, human to human contact, found in soft cheese, hot dog, milk, cold salads.

What is the most likely clinical presentation of the infection with the same
organism in the healthy adult? Mild self-limited gastroenteritis

What is the most likely source of infection in healthy adults? Raw mild; soft
cheese made out of unpasteurized mild, unwashed vegetables, ready to eat
delicatessen meats - hams

What population is under the increased risk to develop serious infection

with
the same organism? Very young or very old, immunocompromised
What is the treatment and prevention of this infection?
Treat ampicillin, prevention – cook the food, avoid soft cheese, peel the
vegetables or wash it

CASE 16
A 19-year-old man is brought to the office for evaluation of a cough and fever.
His illness began 8 days ago with low-grade fever, headache, myalgias, and
fatigue. He now has a persistent hacking dry cough. He has no significant
medical or family history. No family members have been ill recently, but one of
his good friends missed several days of school approximately 2 weeks ago with
“walking pneumonia.” On examination he is coughing frequently but is not
particularly ill-appearing. His temperature is 38.1°C (100.5°F), pulse is 85 beats
per minute, and respiratory rate is 22 breaths per minute. His pharynx is red;
otherwise, a head and neck exam are normal. His lung exam is notable only for
some scattered rhonchi. The remainder of his examination is normal. A chest x
ray shows patchy infiltration. A sputum Gram stain shows white blood cells but
no organisms.

1. What is the most likely diagnosis? List 3 most common causes of

thiscondition;
1.Mycoplasma pneumonia, 2. chlamydia pneumonia, 3. legionella
pneumophilla
2. What Diagnostic and lab tests are helpful in diagnosing this infection?
Chest x-ray, CBC, serologic studies,
 3. Gram staining of the sputum didn’t show any organism; What is
thereason of that?
Most likely its mycoplasma – which doesn’t have a cell wall to stain it
with the gram
4. What is appropriate treatment of this condition? –azithromycin,
doxycycline, fluoroquinolones
5. What are the characteristic symptoms and signs of typical CAP? – The
“typical” community acquired pneumonias described as a sudden
onset of fever, cough with productive sputum, often associated with
pleuritic chest pain, productive cough sometimes rust-colored sputum.
Localized Crackles on chest auscultation and lobar consolidation on the
chest X-ray. This is the classic description of pneumococcal pneumonia

CASE 17
A 23-year-old woman presents with chills, fever and productive cough. 7 days
ago, she developed nasal congestion and myalgia. She became progressively
fatigued and developed cough, productive of 1 teaspoon of yellowish sputum.
Today she saw flecks of blood in it and panicked. Medical history is remarkable
only for appendectomy 2 years ago and a fractured humerus 15 years ago. On
physical exam, she has fever – 39.1°C. Head and neck exam is normal. Crackles
are heard on pulmonary auscultation.

Based on the information given, what is the most likely diagnosis? List 4 most
common bacterial causes of this condition;
Community-acquired pneumonia (CAP)
1. S. pneumonia
2. C. pneumonia
3. M. Pneumonia
4. L. Pneumophila

What are the characteristic symptoms and signs of this condition? • The
“typical” pneumonias described as a sudden onset of fever, cough with
productive sputum, often associated with pleuritic chest pain, and possibly
rust-colored sputum. Localized Crackles on chest auscultation and lobar
consolidation on the chest X-ray. This is the classic description of
pneumococcal pneumonia.
 • The “atypical” pneumonia is characterized as having a more insidious
onset, with a dry cough, accompanying extrapulmonary symptoms such
as headache, myalgias, sore throat, absent or mild findings on chest
auscultation and a chest X-ray that appears much worse than the
auscultatory findings. This type of presentation usually is classic to
Mycoplasma pneumoniae.
• Although these characterizations are of some diagnostic value, it is very
difficult to reliably distinguish between typical and atypical organisms
based on clinical history and physical examination alone.

What Diagnostic and lab tests are you going to order? Which test is
considered to be the “golden test” for to find the causing organism? Best
initial test – Chest X-ray - gives you characterization (lobar, interstitial),
location of inflammatory process (right middle lobe, Left upper lobe, etc.),
presence or absence of pleural effusion. (CT scan is even more informative,
but rarely needed)
• Microbiologic studies - sputum Gram stain and culture - important to try
to identify the specific etiologic agent causing the illness – Most cases are
diagnosed using this method. However, use of this method is limited by
the frequent contamination by upper respiratory flora. Blood cultures can
also be helpful - 30% to 40% of patients with pneumococcal pneumonias
are bacteremia.
• Serologic studies - to diagnose organisms not easily cultured Legionella,
Mycoplasma, or C pneumoniae.
• Nonspecific helpful lab tests that give you information about the general
condition of the patient’s – elevated PMNs, liver and kidney function
tests, serum electrolytes,
• Fiberoptic bronchoscopy with bronchoalveolar lavage often is performed
in seriously ill or immunocompromised patients Gold Standard test for
etiologic diagnosis = biopsy of the lung tissue and culturing the
specimen – invasive; done in very complicated cases that does not
respond to standard antimicrobial therapy

What is the treatment of this condition?

For outpatients without comorbidities - macrolide (azithromycin) or
doxycycline - gives adequate coverage

For outpatients withcomorbiditiesgood choices for treatment of S

pneumoniae, Mycoplasma, and other common organisms:
1. Combination of macrolide with beta-lactam antibiotic OR 2.
Anti-pneumococcal quinolones, such as moxifloxacin or levofloxacin
Hospitalized patients with community acquired pneumonia: 1. usually are
treated with an intravenous third-generation cephalosporin plus a
macrolide OR
2. anti-pneumococcal quinolone - moxifloxacin or levofloxacin

What population has an increased risk of repeated infections with this

organism? What is the prevention?
Asplenia patients, smokers, alcoholics, liver disease – vaccinate

CASE 18
A 31-year-old man presents to the emergency room with 2 days of crampy
abdominal pain relived by defecation, nausea, and diarrhea. He has not had
any blood in his stool. He denies contact with anyone with similar symptoms
recently. The only food that he did not prepare himself in the past week was
scrambled eggs and bacon that he had at a diner the day before his symptoms
started. On examination, he is tired appearing; his temperature is 37.7°C
(99.9°F); and his heart rate is 120 beats per minute when he sits up. His blood
pressure is 110/60 mm Hg when sitting. His mucous membranes appear dry.
His abdominal exam is notable for diffuse tenderness but no palpable masses,
rebound, or guarding. A rectal exam reveals heme-positive stool containing
flecks of mucus.
1. What is the most likely etiologic agent of this infection?
Shigella , dysentery type 1- hus, watery diarrhea - produces shiga toxin which
which inactivates 60S sub-unit ribosomes- inhibtn of protein synth.
Fecal-Oral route.
2. List at least 3 other microorganisms causing the similar
presentation: campylobacter, shigella, salmonella, E. coli
3. What is the diagnostic approach to this patient?
Based history and clinical findings, stool testing for WBCs, blood,
bacteria, CBC, electrolytes
4. What is the management of this patient?
Supportive – fluids, electrolytes; antibiotics for severely ill patients’
ciprofloxacin , flouroquinolone
5. What is the prevention of this infection?
 Adequately cooking the food, washing hands thoroughly while handling
the food
COMPLICATION; hus, arthritis, conjunctivitis, urethritis, intestinal
perforation, seizures in children.

CASE 19
A 20-year-old female is hospitalized with severe symptoms of hemolytic
uremic syndrome. Her medical history is significant for diarrheal disease that
started 3 days prior to development of her current symptoms.
1. What microorganism would most likely be isolated from a stool
specimen?
Enterohemorrhagic E coli (Shiga-toxin producing E. coli – STEC) 0175:07;
2. List the most likely sources that this patient got infected from; poorly
washed vegetables – beef,cucumbers, lettuce, spinach, ham burger 3.
Explain the underlying pathophysiologic mechanism of her current
condition? inhibit protein synthesis of cell binding to Gb3 receptor-inhibits
ribosomes or induces apoptosis.. 4. Describe the symptoms and signs of
hemolytic uremic syndrome; hemolytic anemia, thrombocytopenia, acute
kidney disease.
TTP- HUS symp+ fever encephalopathy. 5. What is the appropriate
management of this patient? Fluids and electrolytes azithromycin,
fluroquinolone
E. pathogenic- infants,
E.aggregative- all
E.invasive- blood, inf colitis.
 CASE 20
A 30-year-old traveler drinks glass of fresh orange juice that he bought in the
street while sightseeing Nepal. Next day he develops watery diarrhea
accompanied by severe crampy abdominal pain. He has no fever; no blood or
mucus is seen in his stool. He is symptom-free in 3 days.
1. What is his most likely diagnosis?
Traveler’s diarrhea - due to ingestion of contaminated wayer, poorly cooked or
unpeeled food.
2. This presentation is typical for which microorganism?
ETEC – enterotoxigenic E. coli - tropical or developing countries.
3. What is the underlying pathophysiologic mechanism of diarrhea in
thiscase?
Bacteria produces 2 toxins: heat-stable toxin – fluid secretion in jejunum
and ileum and heat-labile toxin – structurally similar to cholera toxin 4. What
is the appropriate management of this patient?
Supportive – fluid and electrolytes. Early treatment fluroquinolone, azythromycin.

CASE 21
A 16-year-old male presents with progressive weakness of the legs two
evenings before admission. He has a history of a diarrheal illness 2 weeks
prior. On examination, he has moderate leg and mild arm weakness;
Respiratory function is normal. His muscle reflexes are diminished in arms
and absent in lower extremities. Mental status is clear;
1. What is the most likely diagnosis? Guillain -barre syndrome
2. Describe the underlying pathophysiologic mechanism of this
presentation; antibodies mistakenly attack and destroy the myelin –
weakness and
paralysis results
 3. What microorganism is the most likely because of his current
condition?
Campylobacter jejuni
4. What is the most likely food source that this patient ingested?
Poultry, meat
5. What is the appropriate management of this patient?If necessary,
intubate, plasmapheresis, IV IG

Case 22
A 3-year-old boy presents with “barking” cough and fever. The cough started
suddenly in the middle of the night. On physical examination, the patient’s
temperature is 38.5°C and he appears frightened and anxious. He has a heart
rate of 160 beats/min and a respiratory rate of 36/min. His breathing is
labored and he is using his accessory muscles of respiration. Marked
inspiratory stridor is audible. Lung examination is unremarkable.

1. What is the diagnosis?

respiratory virus infection- para influenza virus.
Symp: turbulent noisy breathing, stredor, steeple sign in xray
2. Which of the most likely viral cause of his symptoms?
Parainfluenzavirus, croup,
3. What is the management of this patient?
Ribavirin, CROUP bed rest,ventilation, glucocorticosteroid.
4. Symptom croup, sore throat, fever, bronclitis, fever, coryza,
horseness,barking cough
5. Diagnosis? Throat swab or nasopharyngeal washing, RT PCR, ELISA.
6. Types: 1croup laryngotracheobronchitis in children
2 similar but mild
3 bronchiolitis and pneumonia in infants
 Case-23
An 11-year-old boy attending summer camp develops sore throat, headache,
fatigue and bilateral conjunctivitis. He is seen by the camp medical staff and on
examination is found to have a slight fever of 37.8oC but no rash. Within the
next 2 days, several of the other campers develop similar symptoms.

1. What is the most likely cause of this infection?

Adenovirus (pharyngoconjunctival fever) symo: sore thr, conjunctivitis, fever,
malaise,cervical adenopathy.
Epidemic keratoconjunvtivitis- pain, punctured corneal lesions,perioccular
adenopathy.
Non resp: cystitis, encephalitis, dairrhea.
2. How is this infection spread?
Contaminated objects, fluid secretions in camps
3. What is the diagnostic approach to this infection?
Throat swab, RT PCR, ELISA , 4 times rise in serum antibody titer.
4. What is the treatment of this infection? Supportive nsaids and
antipyretics.
5. What is the best action to prevent the spread?
vaccination, maintain hygiene
CASE-24
NP is a 29-year-old female from Tbilisi, Georgia presenting to the Emergency
Department in January with 1-day history of fever, myalgia, and rhinorrhea.
Her symptoms are continuous, steadily getting worse. She is having significant
nasal discharge but no cough. She has no significant past medical history, and
takes no medications. 2 of her co-workers have skipped the work recently due
to high fever. Her review of systems is significant for fever, lethargy, nasal
discharge, shortness of breath, and severe muscle soreness. On the physical
exam, she is a well-nourished young woman who is in moderate distress; Skin
is warm, flushed and diaphoretic; Pulmonary exam reveals mild wheezing, no
crackles are auscultated; Abdominal and Cardiac exams are within normal
limits; Mild tenderness upon palpation of extremities; Temperature is 39.4 oC,
Heart rate is 105 bpm; blood pressure is 120/76 mm Hg; respirations 25/min;

1. What is the most likely causing organism of this patient’s

symptoms? Influenza virus : hemagluttinin- site from where
virus binds, neuroaminidase- virus releases DNA.

2. Discuss the epidemiology and pathogenesis of this illness;

children’s adults, immunocompromise patients…. Airborne
droplet, cytokine , IL 1, IL6, TNF, INF IL8

3. List the available diagnostic approaches for this disease;

throat swab, PCR, rapid influenza test

4. What is the appropriate management of this patient?

Antiviral zanamivir-neuraminidase inhibitor

5. Discuss the mechanisms of action of available medications –

acetaminophen, nsaids,Amantadine –block M2 receptor

6. What are the possible complications of this illness?

Pneumonia, cardiovascular disease, pregnancy complications , acute mtocitis.
 7. What is the prevention of this infectious disease?
Annual vaccine.

CASE-25
A 20-year-old student presents to you in January for evaluation of her
respiratory symptoms. 3 days ago, she developed nasal congestion and clear
rhinorrhea accompanied by sneezing. Next day she woke up with malaise and
scratching sensation in her throat. Today on physical exam, the patient is in no
acute distress, but notes fatigue; Head and neck exam is within the normal
limits, pharynx is no erythematous. Her temperature is 37.20C. Lungs are clear.

1. Based on this clinical presentation, what is the most likely diagnosis?

Common cold

May exagerbate- bronchitis, asthama, bacterial sinusitis.

2. What organism is the most likely because of her illness? Rhino virus 3.

How did this patient most likely get infected? Respiratory droplets,

hand to hand contact.

4. Although rarely done, what diagnostic approaches are available to

detect the causing agent? Rhinovirus RNA by PCR, throat swab.

5. What is the management of this patient?

Antipyretics and antihistamines, nasal decongestions.

6. The patient wants to know about the effects of vitamin C and

amoxicillin for her symptoms. What is the adequate response? These
are infective in rhinovirus.
CASE-26
A 20-month-old boy developed fever and irritability 3 days ago. Mother
brought the child to your office today, because of appearance of erythematous
rash. On the physical Exam now, the boy is tired and ill-appearing, he has fever
of 38.7oC. Bilateral redness of conjunctiva and tearing is noted. There is a
brick-red maculopapular rash present on the face and trunk. According to
mother, the rash started on the forehead and spread down and out.

Family- Paramyxoviridae
1. According to the physical exam findings, what is the most
likelydiagnosis? Measles - trnsmission: resp droplets, aerosol. Symp:
fever, koryza, hackig cough, cunjuncyivitis

2. What is the pathognomic feature of this illness?

Kolpik spots- skin rash, bluish white dots on buccul muc and skin.
COMPLICATIONS: otitis media, pneumonia, thrombocytopenic pupura,
encephalitis.
3. Compare similarities and differences between this patient’s illness
andother infectious agents, that should be in your differential
diagnosis; mumps and rubella [in mumps bilateral parotitis and in
rubella lymphadenopathy]

4. What diagnostic tests are available to make the etiologic diagnosis?

Throat swab, serology IgM rise 4 times, RT-PCR

5. What is the treatment of this boy’s illness?Antipyretic, plenty of

fluids, vitamin a

6. What could have prevented development of this infection?MMR

vaccine, 1 dose at 6-15 months, 2 doses at 4-6 year
CASE-27
An 8-year-old boy is brought to your office for evaluation of fever, ear pain, and
swollen cheeks. His mother reports that he’s had 4 days of low-grade fever and
seemed tired. Yesterday he developed the sudden onset of ear pain and
swelling of the cheeks along with a higher fever. He is an only child, and
neither of the parents has been ill recently. He has had no significant medical
illnesses in his life, but his parents decided not to give him any vaccines
because they read that it could cause autism. On examination, his temperature
is 38.6°C (101.5°F), and his pulse is 108 beats per minute. He has swollen
parotid glands bilaterally to the point that his earlobes are pushed up, his
tympanic membranes appear normal. Opening his mouth causes pain, but the
pharynx appears normal. He has bilateral cervical adenopathy.
1. What is the cause of this child’s illness? Mumps- transmittef via resp
droplets, saliva.classic glands- salivary, parotid, pancreas,overies-
oophoritis, testies- epididymid phoritis,cns-aseptic meningitis,breasts

2. What is the prognosis?

Uncomplicated mumps resolve, for meningitis good, deafness, facial paralysis, cerebral
atexis, encephalitis v rare..

3. What diagnostic approach can be used? Clinical findings for meningitis PCR,
ELISA

4. What is the best prevention of this infection? MMR vaccine

5. List the possible complications of this illness; meningitis, encephalitis,

prostatitis, pancreatitis, pneumonia.
6. What is the appropriate management of this child? antipyretic, fluid, apply
ice pack. Finally, vaccine
CASE-28
A 19-year-old woman presents for the evaluation of vaginal discharge that has
progressively increased over the past week. She is sexually active, has had
three lifetime partners, takes oral contraceptive pills and occasionally uses
condoms. On examination, she appears in no acute distress and does not have
a fever. Her abdomen is soft with moderate lower abdominal tenderness. On
pelvic examination, she is noted to have a yellow cervical discharge. No
uterine masses. A Gram stain of the cervical discharge reveals multiple
polymorphonuclear leukocytes.

1. What is the suspected diagnosis? Cervicitis

2. What are the most likely causes of her symptoms?

Chlamydia- replicates in host cytoplasm and gonococcal

3. What is the diagnostic approach to this patient?Vaginal swab, PCR,

ELISA, NAATS.

4. If this condition goes untreated, what complications are likely?

May spread to uterus and fallopian tube resulting in PID which may
cause infertility.

5. Discuss the clinical course of at least 4 complications;INFERTILITY,

HIV, PID, urethritis, reactive arthritis.
6. What is the treatment of this condition?
Doxycycline, erythromycin, tetracycline or single dose azithromycin.

7. What is the prevention of this condition? Protective excuse

condoms, screening.
 CASE-29

A 16-year-old female comes to your office for evaluation of a sore

throat and fever. Her symptoms started approximately 1 week ago
and have been worsening. She has been extremely fatigued for the
last. She denies any ill contacts. She has no significant medical
history, takes no medications, and has no allergies. On examination,
she is tired and ill appearing. Her temperature is 38.5°C. Examination
of her pharynx shows her tonsils to be markedly enlarged and
erythematous. She has prominent cervical adenopathy, which is
mildly tender. A cardiovascular examination is normal, and her
abdomen is soft, nontender, mild hepatomegaly is palpated.

1. What is the most likely diagnosis of this patient?Infectious

mononucleosis - traid- fever, adenopathy, pharyngitis

2. What is the most likely cause of her infection

(cervicaladenopathy, hepatomegaly)? EBV hhv4

3. How is this agent transmitted?

Oral contact kissing, respiratory droplets.

4. what cells in the host does it infect? B cells

5. What is the diagnostic approach to this patient? CBC-WBC

elevated, serology-heterophil antibody test-sheep RBC, EBV
antibody testing.

6. What is the appropriate management of this patient?

Supportive, corticosteroids, avoid splenic rupture.

7. List other conditions associated with the same infectious

agent; Burkitt’s lymphoma, Hodgkin’s disease, gastric
carcinoma, hairy cell leukemia.

CASE-30
A 15-year-old girl presents to her pediatrician with fatigue and a sore
throat of several weeks’ duration. She says that she is still able to
attend classes at her high school but falls asleep as soon as she gets
home. She has never had anything like this before but notes that
one of her close friends has missed school recently. On physical
examination, her vital signs include a temperature of 38.6° C, heart
rate of 72/min, blood pressure of 120/75 mm Hg, and respiratory
rate of 14/min. Her throat is markedly erythematous with occasional
exudates on the tonsils. She has tender posterior cervical
lymphadenopathy bilaterally. Mild hepatosplenomegaly is palpated
on abdominal exam. The remainder of her exam is within normal
limits. A peripheral blood smear reveals atypical lymphocytosis.

What is the most likely diagnosis? EBV - hhv4

What is the pathogenesis of this condition?

Close oral contact with the infected saliva,first infects oropharynx-ATTACK on
B cell of immune system - immune respose of CD8+ t lymp-then virus
remains in b cells in pharynx and asymp interim shredding.

What tests could be used to confirm the diagnosis? WBC

elevated, heterophil antibody test, EBV antibody test- shows IgM.

What is the most appropriate management for this condition?

Supportive, corticosteroids, to prevent splenic rupture - no
heavy lifting..

What are the potential complications of this condition? / What

other conditions are associated with the same virus? Burkitt
lymphoma, Hodgkin disease, gastric carcinoma. anaphylactic
nasopharyngeal carcinoma.

CASE-31
You are called to examine a 1-day-old male because the nurse is concerned
that he is jaundiced. He was born by spontaneous vaginal delivery to a 21-
year-old gravida1 para1 after a full-term, uncomplicated pregnancy. The
mother had no illnesses during her pregnancy; and the only medication that
she took was prenatal vitamins. There is no family history of genetic
syndromes or illnesses among children. The infant is mildly jaundiced and has
several petechias over his abdomen. Inspection is notable for an abnormally
small head circumference (microcephaly). His cardiovascular examination is
normal. His liver and spleen are enlarged. There is no startle response to a
loud noise. CT scan of his head reveals intracerebral calcifications.
Normal CMV- blood, transplant organs, contact with body fluid.recides latently
in, monocytes, dentritic cells and myeloid precursors.

1. What is the most likely cause of this infant’s condition? CMV-hhv5 - most
common cause of non genetical sensorineural hearing loss.

2. How did he likely acquire this infection?

Through vaginal delivery
Most com symp: hepatoslpeenomegaly, jaundice and patachea., blueberry muffin
rashes on skin, Thrombocytopenia, increase glucose in csf, hyperbilirubinemia.

. What is the most common presentation of infection with the same agent in a
healthy adult?
CMV mononucleosis- elevated aminotrasferase, splenomegaly,
leukocytosis.

4. What is the presentation of infection with the same agent in an

immunocompromised host?
Colitis, ulcers, hepatitis, cholecystitis, rhinitis

5. What are the diagnostic methods both in infants and adults?

Virul culture of urine / saliva,CMV DNA by PCR, serology- high Igm and
low IGG (in new infection), culture, biopsy in immunocomp patients.

6. Treatment? Antiviral-Ganciclovir, valaganciclovir or foscarnet.

7. Prevention- prophylaxis of CMV, safe sex.

CASE-33

A 63-year-old man comes to your office for the evaluation of lower back pain.
For the past 3 days, he has had a sharp, burning pain in his left lower back,
which would radiate to his flank and, sometimes, all the way around to his
abdomen. The pain comes and goes, feels like an “electric shock,” and is
unrelated to activity. He has had no injury to his back and has no history of
back problems in the past. He denies fever, urinary symptoms, or
gastrointestinal symptoms. His examination today, including careful back and
abdominal examination, is normal. You prescribe a nonsteroidal anti
inflammatory drug for the pain relief. The next day, he returns to your office
stating that he has had an allergic reaction to the medication because he’s
developed a rash. The rash is in the area where he had the pain the day
before. On examination now, he has an eruption consisting of patches of
erythema with clusters of vesicles extending in a dermatomal distribution
from his left lower back to the midline of his abdomen.

1. What is the diagnosis of this patent? Reactivation zoster- herpes zoster

2. What infectious agent is cause of this rash? hhv3

3. What is the underlying pathophysiologic mechanism of this

infectiousagent causing the disease in this patient?
Latent is dorsal root ganglion and trigeminal ganglion t3 to l2- inflames the sensory
root ganglion..
Infection in trigem nerve can cause severe pain.

4. Describe the clinical features of primary infection with the same

infectious agent; primary infection is macular eruption, papules, vesicle,
pustular, crust. Last 20 days.

5. What is the diagnostic approach to this patient?

Clinical ev,Tzank smear [ giant cell], Confirmatory serology and culture.
6. What is the management of this patient? What is the prevention ofthis
condition?
Wet compresses, analgesics,Symptomatic or acyclovir, vancyclovir, famciclovir
Prevention with2 doses of live attenuated vaccine varicella.
OPthalmic zoster: rash on and near the eye- CN5
Ramsay Hunt synd: CN7 - geniculate ganglion-facial palsy, ear pain, vesicles on
external auditory canal, loss of taste.
CASE-34

A 24-year-old woman presents complaining of 2-days of itchy vaginal

discharge. One week ago, you treated her for a urinary tract infection (UTI)
with sulfamethoxazole and trimethoprim (SMX-TMP). She completed her
medication as ordered and developed the vaginal discharge shortly thereafter.
She denies abdominal pain, and her dysuria has resolved. She is not currently
taking any medications. On examination, she is comfortable appearing and has
normal vital signs. Her general physical examination is normal. A pelvic
examination reveals a thick, curd-like, white discharge in her vagina that is
adherent to the vaginal sidewalls. There is no cervical discharge or cervical
motion tenderness, and bimanual examination of the uterus and adnexa is
normal.

Affects on- skin folds, oral and genital mucosa

Thrush- white patches on skincandida nail infection, candita daiper rashes

1. What is the diagnosis? What is the most likely cause of thispatient’s

symptoms?
Vaginitis cause by candida albican,

2. What is the risk-factors that predispose patients to develop this

condition?
Recent antibiotic use, pregnancy, poor hygiene, diabetes mellitus, hot weather,
restrictive clothing,immunosupression

3. What is the diagnostic approach for this patient’s symptoms?

Koh wet mount, culture, tissue biopsy.

4. What is the appropriate management of her symptoms?

Fluconazole and amphotericin b

5. List the other infections caused by the same infectious agent;

Oral thrush, cutaneous infection, esophagitis, septicemia, endocarditis,
gastritis

CASE-35

A 32-year-old man with known HIV is brought to the hospital with respiratory
distress. He describes increasing shortness of breath over the past 2 weeks
with a nonproductive cough. On physical examination, he is a thin and ill-
appearing man in respiratory distress. He is notably using his accessory
muscles to breathe. Vital signs include a temperature of 38.3° C (101.8° F),
heart rate of 122/min, blood pressure of 122/66 mm Hg, respiratory rate of
34/min, and oxygen saturation of 84%. Auscultation of the lungs reveals
bibasilar crackles with relatively clear middle and upper lung fields. His oral
cavity reveals a white film on his tongue and buccal mucosa.

pCP infects immono comp patients,

Organisms are extracellular- alveolar surfactant abnormalities, increase

alveolar capillary permeability.

Symp: dyspnea, fever, non productive cough, tachypnea, tachycardia,

cyanosis.respiratory alkalosis.

1. What is the most likely diagnosis? Pneumocystis jirovecii

PCP(pnemocytic pneumonia)

2. What risk factors are associated with an increased incidenceof this

condition?
HIV infection cause decrease cd4 count.

3. Below what CD4 count is this condition common? <200/l remain for
three months
4. What prophylactic treatment is generally administered in
suchpatients?
Tmp smx-14 days in non HIV and 21 days in HIV , doc cotrimoxazole + steroids

5. This patient’s CD4 T cell count is found to be 45 cells/mm3. List the

opportunistic pathogens that this patient has an increased risk of;
CMV, mycobacterial avium infection

6. Diagnostic test –broncho-alveolar lavage- increase lactate

dehydrogenase and b-d-glucan, PCR, biopsy, ELISA, lactate
dehydrogenase elevated.
CASE-36
A 38-year-old woman with chronic asthma presents for evaluation of a cough. She has a
history of asthma for most of her life and is managed with inhaled bronchodilators and
inhaled steroids. 3 days ago, she developed a cough productive of brown mucous and,
occasionally, blood. She has a low-grade fever as well. Her asthma control has been
significantly worsened since she developed the cough. On examination, she has a
temperature of 37.7°C and a respiratory rate of 22 breaths per minute, and her
saturation of oxygen is slightly low (96% on room air). She is coughing frequently. Her
head and neck exam are unremarkable. Her pulmonary examination is notable for
diffuse expiratory wheezing. A chest x-ray shows a lobular infiltrate that is reminiscent
of a cluster of grapes. A complete blood count (CBC) shows a mildly elevated white
blood cell count with a markedly elevated eosinophil count. A microscopic examination
of her sputum is also notable for the presence of numerous eosinophils. Her Ige levels
are strikingly high. You suspect fungal etiology of her worsened symptoms.
Symo: fungus ball- fibrous tissue, cough, hemoptysis, wheezing , mild fatigue,
erythmatous rashes, hemm infarcts, cystic fibrosis, eosinophils, elevated IGG

What is the most likely diagnosis? aspergillosis - infects previously cavitated lesions like
tb, sinuses.

What fungus is most likely causing her symptoms? Aspergillus fumigates

Describe the morphologic characteristics of this fungus;

One of the most common environmental molds- present on decaying plants,
branches of trees, insulating materials, airconditioners and heaters.
color of steps - grey around apex, smooth surface, small columnous globose -
forms spore and is transmitted via inhaling the spores.

What are the risk factors for acquiring this fungus?

Neutropenia, long- term corticosteroid therapy, AIDS, Organ transplant(specially bown
marrow).

List different forms of disease caused by the same fungus; invasive

aspergillosis, allergic bronchopulmonary aspergillosis, superficial aspergillosis,
endocarditis, chronic granulomatous sinusitis

List the helpful diagnostic approaches to diagnose infection with this fungus
positive culture and sputum culture,
CXR – halo sign, aspergillus antigen test, biopsy of nodules , sputum culture

Tx- voriconazole OR amphotericin B,

Prevention – discontinuation of corticosteroid therapy
CHRONIC GRANULOMATOUS SINUSITIS: facial swelling and unilateral ptosing

CASE-37
A 59-year-old male presents to your office for follow-up of some abnormal
blood test results. His liver enzymes are elevated by approximately three times
the upper limits of normal. The patient denies alcohol or drug use and is not
taking any medications. He gives no history of jaundice. His past medical
history is significant only for hospitalization at the age of 35 for a bleeding
stomach ulcer. He required surgery and transfusion of 5 units of blood. His
physical examination is normal: it shows no signs of jaundice, no
hepatosplenomegaly, and no findings suggestive of portal hypertension. You
suspect an infectious etiology;

1. What is the most likely infectious cause of his abnormal liver

functiontests?
Hepatitis c virus

2. How did he most likely acquire this infection? Blood transfusion from
past past history

3. Discuss the epidemiology of this infectious agent: What are

thetransmission routes, what population is under increased risk of
having this infection, who needs to be screened
organ transplant patients, health care worker.
4. What is the prevention- safe excuse of double gloves by HCW? Avoid
needle injection in drug abuser, 90% by transfusion. hemodialysis,
injection drug user, organ transplant.
5. Describe clinical course characteristic to the suspected infectiousagent;
infection leads to chronic liver disease.

6. Treatmentsofosbuvir/ledipasvir, Grazoprevir

7. What diagnostic tests are you going to order to find out the exactcause
of his abnormal liver function tests?
Anti hep c assay, HCV RNA PCR.

Case 38
A 26-year-old man comes to your clinic complaining of a 5-day history of
nausea, vomiting, diffuse abdominal pain, fever and muscle aches. He has
lost his appetite, but he is able to tolerate liquids and has no diarrhea. He
has no significant medical or family history, and he has not traveled outside
the country. He admits to having 12 different lifetime sexual partners, denies
illicit drug use, and drinks alcohol occasionally, but not since this illness
began. He takes no medications. On examination, his temperature is 38°C °F,
heart rate 98 bpm, and blood pressure 120/74 mm Hg. He appears jaundiced,
his chest is clear to auscultation, and his heart rhythm is regular without
murmurs. His liver percusses 4 cm below the costal margin and is smooth
and slightly tender to palpation. He has no abdominal distention or
peripheral edema. Laboratory values are significant for a normal complete
blood count, creatinine 1.1 mg/dL, alanine aminotransferase (ALT) 3440 IU/L
(normal: 7 55 U/L), aspartate aminotransferase (AST) 2705 IU/L (normal: 8 -
48 IU/L), total bilirubin 24.5 mg/dL (normal: 0.1 - 1.2 mg/dL);
What tests are going to order to find the exact infectious cause of your
patient’s disease? Explain why;
serological test
Recovery phase - HBsAb +ve, anti HBc IgG +ve
Chronic phase- HBsAg +ve upto 6 months, anti HBeAg +ve
Window phase-anti hbc + ve
Vaccinated – HbsAb +ve and anti HBc –ve.
Discuss the transmission modes and prognosis for each possible
infectious cause of this patient’s symptoms:
Hepatitis A fecal - oral (100 percent recovery)
Hepatitis B sexual transmission, mother to fetus. Less by transfusion 90
percent recovery 5 percent chronic
Hepatitis C blood transfusion, iv drug abuser. Less by trans placentally. 85
percent chronic
Hepatitis E fecal oral 100 percent

Treatment :- entecavir, tenofovir other are interferon alfa, lamivudine,

adefovir.
Prevention:- hbv ig g with in 48 hour.

CASE 39
A 34-year-old man is brought to the clinic for a 3-month history of
unintentional weight loss (6kg). His appetite has diminished, but he reports
no vomiting or diarrhea. He does report some depressive symptoms since the
death of his wife a year ago, at which time he moved from Kiev to the United
States. He admits night sweats. He denies a smoking. He complains of a
3month history of productive cough with greenish sputum. He has not felt
feverish. He takes no medications. On examination, his temperature is 380C
(100.4°F) and respiratory rate is 16 breaths per minute. His neck has a normal
thyroid gland; no cervical lymphadenopathy is noted. Supraclavicular
lymphadenopathy is palpated on the left side. His chest has few scattered
rales in the left upper-lung fields. His heart rhythm is regular with no gallops
or murmurs. His abdominal examination is benign and his stool is negative for
occult blood. His chest x-ray shows left upper lobe cavitary lesion.

1.What is the most likely diagnosis and what is the causing organism? What
is the underlying pathophysiologic mechanism of the disease? • Pulmonary
tuberculosis (TB) - Mycobacterium tuberculosis • Granulomatous lesions are
caused by the inflammatory response of lymphocytes and macrophages. T
helper cells activate macrophages by production of INF-gamma. Macrophages
encircle the lesion and control the spread of infection - The center of the
lesion may become necrotic (caseous necrosis) and form a cavity. Sometimes
it may get calcified, healed lesions are called Ghonlesions. (Ghon complex –
granulomatous necrosis of the pulmonary lesion + same process in the lymph
node) Most patients exposed to M tuberculosis do not manifest clinical
symptoms, but they may have a latent infection. Years later, frequently during
times of stress or immunosuppression, TB may reactivate and become
symptomatic.
Reactivation TB usually involves the apical and posterior segments of the
upper lobes or the superior segments of the lower lobes of the lungs.

2. What is the clinical course of this disease? What are the characteristic
symptoms and signs of the infected patients?
Signs and symptoms are nonspecific and subacute, including fever, night
sweats, malaise, unintentional weight loss, and anorexia. The cough usually
is productive of purulent sputum and sometimes streaked with blood.
Cervical and supraclavicular lymphadenopathy – sometimes.
3.What is the diagnostic approach to this patient?
X-ray, CBC,
• The diagnosis of TB is made by combining the history and clinical picture
withAcid-Fast stains or culture of a specimen (smear or tissue
biopsy).Sputum samplesfor identification of the organism, and for
culture. Cultures may take from 4 - 8 weeks.
• Purified protein derivative (PPD), or tuberculin skin testing - useful for
screening for latent TB infection but has a limited role in diagnosing
active infection because of frequent false-negative results. A positive PPD
is defined by induration of at least 5 mm after 48 to 72 hours
➢ HIV-infected persons or persons receiving immunosuppressive therapy
≥5 mm
➢ Close contacts of tuberculosis patients ≥5mm
➢ Persons with fibrotic lesions on chest radiography ≥5mm
➢ Recently immigrated persons (≤5 years) ≥10
➢ Persons with high-risk medical conditions≥10
 ➢ Low-risk persons≥15
• Interferon-gamma release assays (IGRAs) are the most specific diagnostic
tools for latenttuberculosis. They measure T-cell release of interferon-
gamma (IFN-gamma) followingstimulation by TB antigens. All patients
with positive PPD should undergo IGRA testing - The most commonly
used IGRAs are the QuantiferonTB Gold assay.

4. What is the treatment approach for this patient?

therapy generally starts with a 2-month course of four-drug treatment with
isoniazid(INH), rifampin, pyrazinamide, and ethambutol, followed by 4
months of INH and rifampin. Multiple drugs are used to avoid resistance.
Pyridoxine (Vit. B6) is added to the regimen to avoid neuropathy caused by
INH

5. What is are the side-effects of the medications used in first-line therapy?

➢ isoniazid(INH) – Hepatotoxicity, peripheral neuropathy
➢ Rifampin – Hepatotoxicity, orange body fluids, autoimmune
thrombocytopenia
➢ Pyrazinamide – Hepatotoxicity, hyperuricemia, arthralgia, gouty arthritis
➢ Ethambutol – Hepatotoxicity, optic neuritis, green color blindness

CASE 40

A 7-year-old girl is brought into the office for evaluation of a sore throat and fever,
which she has had for approximately 4 days. Her parents have immigrated to the
United States from Russia about 4
months ago. She has not had much medical care in her life, and her
immunization status is unknown. On examination the child is anxious, tachypneic, and
ill appearing. Her temperature is 38.6°C (101.5°F), and her voice is hoarse. Examination
of her pharynx reveals tonsillar and pharyngeal edema with the presence of a gray
membrane coating of the tonsil, which extends over the uvula and soft palate. She
has prominent cervical adenopathy. Her lungs are clear.
1. Based on this clinical presentation, what is your primary diagnosis? What is the
most likely causing organism? If your diagnosis is correct, what could have prevented
this presentation? pharyngeal diphtheria caused by cornybacterium deptheria. –
vaccination dtp

2. The causing microorganism has a major virulence factor - an exotoxin. What is

the mechanism of action of this toxin?

Spreads through aerosol, mostly in children,

First in pharynx- spreads systemic thats why is toxemic and not bacteremic.
Settles in tonsils and uviela-toxins releasedinflammation-psuedomemberane
formation-greyish white membrane-into pharynx and larynx (causes massive neck
swelling and edema-bull neck appearaance)
Toxins bind to EF2 proteins-tranlocation transmmination-

3. What complications may follow?

Toxin – neurotoxic, cardiotoxic – weakness and arrhythmias, cardiomyopathy;
sloughing of the pseudomembrane - fatal airway obstruction

4. What is diagnosis of your suspected condition? Culture from the site of

infection, demonstration of characteristic histopathology - chinese letter pattern

5. What is the management of this patient? Antitoxin as soon as possible,

antibiotics penicillin and eryrhromycin

CUTANEOUS DEP: punced out , hollow ulcers on arms which form

pseudomemberane- caused by organism itself and not toxin.

CASE 41

A 16-year-old male presents with progressive weakness of the legs

two evenings before admission. He has a history of a diarrheal illness
2 weeks prior. On examination, he has moderate leg and mild arm
weakness; Respiratory function is normal. His muscle reflexes are
diminished in arms and absent in lower extremities. Mental status is
clear;

1. What is the most likely diagnosis?

 Guillian-barre syndrome caused by Compylobacter. Jejuni

2. Describe the underlying pathophysiologic mechanism of this

presentation; antibodies mistakenly attack and destroy the
myelin –immunologic demyelinaion of peripheral nerves
causing ascending paralysis; 15% develop respiratory muscle
paralysis – require ventilator

3. What microorganism is the most likely cause of his current

condition? Campylobacter jejuni

4. What is the most likely food source that this patient ingested?
Raw and undercooked meat (Poultry)
5. What is the appropriate management of this patient?
Azithromycin (classic choice) If necessary, intubate;
plasmapheresis, IV IG

CASE 42
A 39-year-old construction worker presents with symptoms of jaw
discomfort and dysphagia that started yesterday evening. Today he
woke up to discover that his symptoms have been worsened. Now
he also complains of stiffness in his neck, back, and shoulders. On
examination, he is unable to open his jaw, his proximal limb
muscles are stiff as is his abdomen and back, but the hands and feet
are relatively spared. He occasionally has violent generalized muscle
spasms that cause him to stop breathing, but there is no loss of
consciousness. His muscle reflexes are exaggerated.
Fixed jaw and eyebrows are elevated, bruce lee- rocky like tetanus
spasm of muscles of abdomen, neck and back- patient is unable to
speak and cry., cyanosi- repiratory arrest.
Mortality is highest at greter age and drug abusers.

1. What bacterial agent is responsible for his symptoms?

Clostridium tetanus (LOCK JAW)

Titanus neonatorum- tetanus from umblicus.

2. Explain the underlying mechanism of his clinical
presentation? toxin tetanospasmin inhibits release of
inhibitory
neurotransmitter – GABA; excessive stimulus to muscles –
tonic spasm and spastic paralysis , once toxin bound cannot be
neutralised.

3. What is the most likely source of his infection?

dirty puncture wounds, soil, rust - is laible for years.
4. What could have prevented development of this
presentation?
DTP vaccine – preexposure prophylaxis; post exposure –
toxoid; tetanus immunoglobulin
5. What is the appropriate management of this patient? Debride
the wound, human tetanus immunoglobulin and tetanus
toxoid,benzodaisapine for muscl spasm, supportive care –
intubate, give benzos, quiet room, bladder catheter, breathing
exercises
CASE 43
5-year-old male is brought by his grandmother for the routine check
up. The child was born to a mother who did not receive any prenatal
care. He is known to have hearing difficulties. On the physical exam,
you notice that his nasal cartilage is somewhat depressed(saddle
nose). His upper incisors are centrally notched and widely
spaced(Hutchinson’s teeth); His molars have
more than usual cusps- mulberry molar . His shins are deformed.
 1. What is the most likely diagnosis of this child?
Whatmicroorganism can be the cause of this presentation?
Congenital syphilis – treponema pallidum.

2. Although not seen in this child, what are the other

findingsalso associated with the same disease? Early signs –
rhinitis – snuffles, mucocutaneous lesions, bony chnges,
hepatospleenomegaly, thrombocytopenia, jaundice, anemia,
lymphadenopathy.

Late changes: 8th nerve deafness, neurosyphillis.

3. What could have prevented this presentation in this child?

Screening and treatment of mother during pregnancy

4. What is the clinical course of the infection with

thismicroorganism if it infects an adult?
Stage 1 chancre – painless ulcer on genitals; painless
inguinal lymphadenopathy; stage 2 – papulosquamous
generalized rash, condyloma lata,
generalized lymphadenopathy; latent syphilis; tertiary
syphilis: neurosyphilis, cardiovascular, or gummatous syphilis
.

5. What is the treatment of this infection in an adult? Penicillin

-1stchoice, doxycycline in allergic patients, in pregnancy or
neurosyphilis – penicillin; if allergic to penicillin, desensitize
and give penicillin.
CASE 44
A 43-year-old woman presents to the emergency room with a 2-day history of
severe diarrhea and vomiting. Her symptoms started shortly after returning
from a trip to a rural area in Somalia. She recalls drinking un-boiled water. Her
symptoms started abruptly, with watery diarrhea followed by vomiting. She
denies abdominal pain. On examination, her temperature is 37.2°C (98.9°F),
pulse is 115 beats per minute, and blood pressure is 80/50 mm Hg. Her
mucous membranes are dry, and her eyes appear sunken. Her skin is dry and
tents when lightly pinched. Her abdomen has hyperactive bowel sounds but is
nontender. Her stool is watery and tests negative for blood. A metabolic panel
shows hypokalemia and low serum bicarbonate;
Symp: waterry dair- rice water stools, sever water and electrolyte depletion,
thirst, oliguria, muscle cramps,weakness, metabolic acidosis with K+
depletion.
IF CHOLERA UNTREATED=- Circulatory collapse.

1. What organism is most likely cause of this patient’s symptoms?Vibrio

cholera - entero toxins and then fluid secreted by it.
Occurs when warm atm, high susceptibility in children, blood type O.

2. What is the underlying pathophysiologic cause of thispatient’s

diarrhea?
Toxin stimulates cAMP- activatesCFTR(cystic fibrosis trnsmembrane
regulator) -increase ion and watery dairrhea, inhibition of NACL
accumulates water and then forms watery dairrhea.

3. What is the appropriate diagnostic approach to this case? – stool test,

isolation of bacteria, CBC, electrolytes , serum creatinine and BUN
should be measured.

4. What is the appropriate management of this patient? Fluid and

electrolyte supplementation – major-K+ can be aded to the solution. ,
antibiotics – quinolones, doxyclin – might be helpful if started early

5. What are the measures to prevent this disease? Boil the water in
endemic areas, avoid drinking water contamination with stool, boil
water, maintain hygiene., whole cellB subunit vaccine.

CASE 45

A 52-year-old man presents for the evaluation of diarrhea and abdominal pain,
which have been worsening over the past week. He is now having 8–10 watery
stools a day and mild cramping pain. He denies vomiting, fever, ill contacts, or
having had blood in his stool. He has no history of gastrointestinal diseases. He
states that approximately 10 days ago he completed a course of
amoxicillin/clavulanate for sinusitis. On examination, he is mildly ill
appearing, but his vital signs are normal. His abdomen is soft, has hyperactive
bowel sounds, and is diffusely, mildly tender.
 1. What is the most likely etiologic agent of this disease?
Clostridium difficile (Abx associated colitis) extreme age, sever
underlying disease, prolonged hospital stay, nursing home.

2. toxins- enterotoxins and cytotoxins

Highest risk: clyndamycin, cephalosporins 3rd gen, floroquinolones.

2. What condition predisposes this organism to cause disease inhumans?

Why?

Coming in contact with health co workers,uncommon env- soil, water.

Antibiotic use – antibiotics kill the normal flora in GI especially colon,
this bacterium is resistant to most antibiotic and outgrows – fluid
secretion causes diarrhea and pseudomembranous colitis; found
commonly in soil, water and household pets

3. What can sometimes be found with the colonoscopy/sigmoidoscopy? –

pseudomembranes colitis.
Toxic Mega colon in rare cond, reactive arthritis is seen.

4. What is the appropriate diagnostic approach to this patient?PCR/culture

of the stool stool, sigmoidoscopy/colonoscopy, diarrhea (3 unformed stools
x2/day w/o other cause) + toxin in stool toxin

5. What is the management of this patient’s diarrhea?Discontinuation of

the Abx, metronidazole for 10 days (mild to moderate); vancomycin or
fidaxocin (severe sx.), check – if still present – 10 days of metronidazole,
if still present – vancomycin; colectomy for fulminant CD infection

6. Complications? Toxic megacolon, reactive arthritis

CASE 46
A 26-year-old man who started working as a veterinarian 6 months ago,
presents to your clinic with the complains of low-grade fevers, generalized
malaise and increasing fatigue for 4 months. On the physical exam, he appears
mildly ill, is in no acute distress but notes having chills. His temperature is
37.3oC. A low pitched cardiac murmur is auscultated; Lung exam is normal.
Cardiac ultrasound show valvular vegetations; Repeated blood cultures grow
no organisms.

1. What is your primary diagnosis? Subacute endocarditis

 2. Which microorganism is the most likely to be the cause of his
symptoms? coxiella bunetti – veterinarian

3. List other microorganism capable of causing similar presentation;

HACEk group, bartonella species

4. What tests can be used to diagnose the suspected infection? Serology,

PCR of the material taken from the heart valve

5. What empirical antibiotic therapy is recommended? Gentamicin,

doxycycline, ceftriaxone

CASE 47
A previously unvaccinated nurse incurs a needle stick from a
patient with known active hepatitis B infection.
1. What is the appropriate management for the health
careworker?
Single dose hep b immunoglobulin +3 doses of hep vaccine
within 1 week of exposure.

2. What are the symptoms and signs of acute viral Hepatitis?

Jaundice, abdominal pain, dark urine, headache, fatigue.

Polyarthritis nodosa,
 3. What viral proteins are used for serologic diagnosis of
HBVinfection?
envelop antigen antibody, Hepatitis B surface antigen, Hepatitis
B surface antibody, hepatitis B core antibody.
4. What are the transmission routes of HBV?
Sharing needles, sexual contact, transplacental, blood
transfusion.
After that HBV is attached to liver cell surface- tlyph
and CD8+ cells rec- destroy process intn Antigen-
antibody complex dep in glomglomerulonephritis,

5. What are the complications of HBV?

Fulminant hepatitis, serum sickness like syndrome, chronic
hepatitis.
Anti HBc is only marker of window phase of hepatitis B.
Igm- ongoing
Igg- recovered.

6. What is the prognosis of the HBV infection?

Is good 95% recover, only 5% ptns goes to cirrhosis if left
untreated. Give entecavir or tenofovir.

CASE 48
A previously healthy 21-old college student is admitted with the complaints of
blurry vision and dry mouth that started 1 hour ago. He no longer can hold his
eyes open and pupils do not react to the light. He’s afebrile, and does not
report headache, or neck stiffness. His medical history is insignificant other
than appendectomy 10 years ago. Last meal was in the morning when he
opened the jar of home-canned sun-dried tomatoes sent by his mother. He
recalls no sick contacts. He lives alone in the dormitory room. He does not
smoke cigarette, but reports occasional marijuana and beer use on weekends.

What is the most likely diagnosis? What is the cause of his symptoms?
Describe the organism responsible for this patient’s symptoms How did this
man get “infected”?
Botulism – ingestion of preformed toxin- neurotoxin-blocks the release
of acetilcholin fron nerve terminals- Flaccid paralysis, chlostredium
botulinum – anaerobe, spore forming(highly heat resistnt) - food borne
Other types: wound born- infected tissues :
infant- large intestine of infants.
Injecting contaminated heroin in the muscle and skin- most risky

What role does this substance have in cosmetics? – wrinkles, strabismus, etc

What are the symptoms and How is this disease diagnosed? Nausea,
vomiting, cramps, diarrhea followed by neurologic symptoms. Muscle
weakness: starts in cranial nerves and is descending, bilateral symmetric,
double vision, drooping eyelids, blurred vision, slurred speech, difficulty
swallowing, decreased gag reflex, constipation, no fever
• Diagnosis: Clinical + suspicious food source; confirmed by: botulinum
toxin in serum, stool or food

What is the underlying pathophysiologic mechanism of this disease?

Block of Acetylcholine release form the presynaptic nerve terminal

What is the management of this patient? What is the treatment?

Respiratory muscle paralysis – cause of death – hospitalization and close
monitoring – if necessary – intubation;
Antitoxin – binds only to unbound toxin, cannot neutralize to toxin already
bound; should be administered as soon as possible

What are the other forms of the disease and how can someone develop this
condition?
• Infant botulism – ingestion of botulinum spores, mostly spontaneous,
sometimes due to ingestion of contaminated hone. Honey is strictly
contraindicated in infants <12- muscle weakness, constipation followed
by neuromuscular paralysis, poor gag reflex, poor oral secretions. Tx-
antitoxin, immunoglobulin.
• Wound botulism – history of deep puncture wound, same neurologic
symptoms, no GI symptom
Comp: daiphram paralysis, pulmonary infection.
TREATMENT: Antitoxins(A,B,E), diaphragm paralysis- intubation.
PREV: vaccine, heating of home canned food before serving
 CASE 49
A 53-year-old man, a recent immigrant from Vietnam, is brought to the
emergency room with a cough productive of bloody sputum. He first noticed a
cough approximately 2 months ago, but there was not much sputum. In the
past several days his sputum production has increased and become mixed
with blood. He reports having lost approximately 5kg in this time frame as
well. He also notes that he’s had drenching night sweats 2 or 3 nights a week
for the past month. He has a 50-pack-year smoking history but no other
medical history. He came to the United States from Vietnam 7 months ago. On
examination, he is a thin, frail-appearing male. His vital signs are normal. His
head and neck exam is normal. He has no palpable adenopathy in his neck or
axilla. His lung exam is notable only for decreased breath sounds diffusely. A
chest x-ray shows a cavitary infiltrate of the right upper lobe.

1. What is the most likely diagnosis? What organism is likely cause of

thispatient’s presentation?
TB – mycobacterium tuberculosis- rod shaped.

2. What is the microbiologic characteristics of the organism, suspected

tocause the disease?
 Acid fast organism, cell wall composed of mycolic acids,They are acid fast.

3. Describe the ongoing pathologic and immunologic processes in

thispatient; TB-INHALED-goes in the lungs-body immune respose- wbc
engulf bacteria but bacteria resistes fusion of lysosome and
replicates(Granuloma formation)-gorhn focus-ghorn complex
formation(gorh cavity+hilar lymphnode inv)- caseous nec-tissue(delayed
type imm hypersensitivity) opacification and cavity on x-ray.Pleural
effusion.

4. What is the appropriate diagnostic approach to this patient?

Tuberculin skin test, IGRA-iterferon gamma release assay,blood test for Tb, lung
bipsy, x-ray, CT, nuclic acid amplification, baceria culture

5. What is the first-line treatment of this patient? What is the duration

ofthe therapy?
2 months all 4 drugs, 4 months of isoniazid and rifampin #SIDE
EFFECTSNeuropathy,optic neuritis, gout, photo sensitivity,orange body fluid.
TB bacteria may remin laten- activate when the patient is immunocomp(eg-hiv ,aids)
Activates-forms cavities-spreads to other organs-BraiN-meningitis, KIDNEY-pyurea,
LUBAR-Potts disease, ADrenal glands-addisonCEVICAL LYMP-N- Lymphadenitis.

EXTRA QUESTIONS

A 56-year-old man is having intermittent fevers and malaise for the past 2
weeks. Two months ago, he had aortic valve replacement surgery. His
postoperative course was uncomplicated. On examination, his temperature is
38°C, blood pressure 124/80 mm Hg, pulse 72/min, and head and neck are
normal. The second heart sound is mechanical, and a 2/6 early diastolic
murmur is heard. Which of the following is the most likely causative organism
ohis condition?

A 31-year-old patient from Indonesia presents to your office with the 2

months’ history of painless supraclavicular lymphadenopathy, malaise, low
grade fever, weight loss and night sweats. For the last 2 days, his symptoms
are accompanied with the numbness and tingling of the lower extremities.
MRI of the vertebral column is shown on the slide. Which of the following is
the most likely combination of the diagnosis and management?

A 5-year-old boy with no vaccinations is brought to ER with a 10-day history of

coughing and choking spells. The WBC count is elevated with 90 % of
lymphocytes. The child is gasping for air, is experiencing paroxysms of
coughing and vomits because of forceful cough. What is the most likely cause
of the child’s symptoms?

A 9-year-old child is brought to the emergency room with the chief complaint
of enlarged, painful axillary lymph nodes. The resident physician also notes a
small, inflamed, 5 Tetri-sized lesion surrounding what appears to be a small
scratch on the forearm. According to the aunt, the child was seen playing with
kittens and puppies. The lymph node is aspirated and some pus is sent to the
laboratory for examination. Staining reveals many highly pleomorphic, rod
shaped bacteria. The most likely cause of this infection is: LYME DISEASE

HIV: human immunodeficiency virus- AIDS(aquired immunodeficiency

syndrome) Kaposi sarcoma, JEVERNII pneumonitis infection., oral candidiasis,
EBV, esopagiis, hrpes zoster.

HIV1-M,N,O,P- cause of AIDS. HIV2-A through H.

Tansmmission: Sharing used needles,blood transfussion, oral anal sex- most

common(accumulates in semen), occupational- helath care workers

Risk: ulcerative STI, unprotected sex,HBV & HCV, Mother to child- 2nd &3rd
trim, during birth , brest feeding.

#- antiretroviral therepy- reduces risk of HIV by reducing plasma viremia.

ENZYME: reverse transcriptase-RNA dependent DNA polymerase.

REPLICATION; phase1- virus enters host cell through specific cell surface
receptors. Phase2- virus introduces RnA and enzyme RTase and forms dsDN~A
Integration is permanent.
1)The reverse transcriptase
2)The integrate
3)The protease

Life cycle- viral gp120 binds to the host CD4 cells, t lymphocytes,
macrophages.
Two majr host co proteins- CCR5, CRCX4
Gp120-fuses with host cell receptor-reverse transcriptase coverts RNA to DNA-
DNA goes to host DNA and HIV assembly- new viral particle foration.
If virus succesfully goed into lymphnodes then the infection is irreversible

Acute HIV synd: viremia and diseminession of virus.

Symtoms; lymphedenopathy, herglobulinemia, severe weight loss

 IMMUNE RECONTsTITUTION INFLAMATORY SYNDROME: 2 to 4 weeks aftr
intitaton of anti retrieval thrpy cART Graves disease, ymphadnitis,
hepatitis,uvieitis,sarcoidosis.: treatment-Glucocorticoids. DAOGNOSIS of HIV:
ELISA+ Western Blot- gold strand- p24 antigen, Rt-PCR.

TREATMENT: neucleotide reverse transcriptase inhibitors- stavudine, abacvir,

protease inhibitors- lopinavir,indinavir, fusion inhibitors , integrase inhibitors.

Prevention- bcg vaccine.

KAPOSI SARCOMA- causative agent is Hhv 8- virus attacks, macrophages, B

lymphocytes , endothelial and epithelial cells.

HSV- HSV1: gangivostomatitis, ecteritis, labialis.

HSV2: mostly genital.

TRANSMISSION: from close person who is actively shredding virus.

If untreated- incubation in nerve ganglia and can cause secondary infection.

HSV1: Primary infection- gangvinal and oral ulcers

: Secondary- Labialis- ulcers on lips(cold sores)

DAIGNOSIS: Clical evolutin- pregnant or not?,

Immunocompromised, severe infection.
Tzanc test: scraping of ulcer- mutinucleated giant cell, viral culture.
IF IMMUNOCOMPTOMISED-HIV SHOULD BE SUSPECTED

TREATMENT: Acyclovir , valacyclovir, Symptomatic- analgesics.

RUBELLA: spreads by respiratory droplets.

Primary replication in naspharynx , then spreads to the lymph nodes

SYMPTOMS: low grade fever, malaise, lymphadenopathy, occasional arthralgia, rash- begins at
the face and neck then travels to the trunk.
In adults- fever , malaise, artralgia, rhinitis, arthritis, stiff joints,

CONGENITAL RUBELLA:primary maternal infection during pregnancy- 16 w of

gastation. Invades placenta-endothelial blood vessel damage- lysis of tissue-mitosis
imp. Symp; most frequent in eyes, ears, heart: Cataract, hearing loss, micocephalitis,
hepatospleenomagaly,PAD, IUGR,dermal erryth- blueberry muffin baby.

DAIGNOSIS: maternal rubella screening, viral isolation of amniotic fluid, infant body titters.
TREATMEnTS: no specific treatment, no immunoglobulins, observation, symptomatic evolution.
PREVENTION: MMR vaccine-2 doses- 1) 12-15 mo 2) 4-6 years.

CHICKEN POX; varicella zoster. Hhv3

Extremely contagious- spreads via droplets.
After aute infection virus goes in latent stage- posterior root ganglion.
Epi- winter and earlr spring
Symp: headache, fever, malaise, lesions develop on face and trunkmacul-pappule-vesicles-
pastul-crust., pain while swallowing
Complication: sec bacterial inf-strep, stephylo, pneumonia, myocarditis, arthtritis,
Reye’s syndrome- dev after 8-10 days of rashes- Hepatitis, encephalopathy, headache, vomiting,
confusion- increases treatment with aspirin.
Daig:Clinicle ev, immunoforosence, serology
Tretment- Antihistamines, acyclovir, valacyclovir.
Prev: antiviral ther, vaccine.- contra ind- pregnent women, patient with severe disease,
immunocomp