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OLEMISS / OTHER / Phcg 321 / What is the pathogen in pulmonary?

What is the pathogen in pulmonary?

What is the pathogen in pulmonary?


School: University of Mississippi
Department: OTHER
Course: Pathogenesis of infectious diseases
Professor: Marc slattery
Term: Fall 2017
Cost: 50
Name: case studies pathogenesis
Description: summarized case studies. refer to book for deeper understanding
Uploaded: 11/29/2017
13 Pages 19 Views 3 Unlocks


What is the pathogen in pulmonary?

Case study

non-productive cough, nasal stuffiness, and fever. Severe muscle aches, joint pains, and generalized headache

Epidemiology​: recently visited grandchildren who all had high fevers & complained of muscle aches.

Physical​ ​exam:​ ​positive findings in

- Temp. 39 C

- Throat

- Erythematous

- Nasal discharge --- clear

- Muscles -- diffusely​ ​tender

- Chest x-ray (CXR) --in normal limits

3 days later, slight improvment in muscle aches, cough & joint pain

4th​ ​day developed​ ​high​ ​fever​ ​(40 C) included teeth​ ​chattering​ ​chill.​ ​Cough​ ​became productive​ ​w/​ ​a​ ​rusty​ ​colored​ ​opaque​ ​sputum,​ ​short​ ​of​ ​breath

What is the treatment for pulmonary?

Repeat of physical​ ​exam:​ ​temp of 40.6 C, respiration rate of 36 per min...ill-appearing, anxious, percussion with E-to-A changes, and rales and rhonchi localized in left lower lobe. Peripheral​ ​WBC​ ​measured:​ ​16,000mm^3, with 68% PMNs, 20% immature forms, 8% lymphocytes, and 4% monocytes.

Sputum​ ​gram​ ​stain:​ ​gram-positive lancet-shaped diplococci, many PMNs and no squamous epithelial cells Don't forget about the age old question of What is the difference between an interest group and a political party?

CXR:​ ​dense left lower loba and lobar infiltrate

Disease:​ ​pneumococcal pneumonia

Pathogen:​ ​streptococcus pneumonia

Typical signs that will indicate pulmonary

What are the five radiologic cxr patterns?

Don't forget about the age old question of What is the kelvin scale of daylight?
If you want to learn more check out What is the keynesian model?

Symptoms​: cough, chest discomfort, rigor, shortness of breath, epideimeology Diagnostics​: CXR, sputum gram stain, WBC count/blood culture Don't forget about the age old question of What are the science of behavior and mental processes?

Treatment​: penicillin, Amoxicillin, fluroquinolones, vancomycin

Typical​ pathogens​: streptococcus pneumonia, haemophilus influenza, staphlyococcus aureus, legionella pneuomophila

Key​ ​points:​ ​about the classification of pneumonia

● Pace of illness 

○ Acute​ - symptoms develop over 24-48 hours

○ Chronic​ - symptoms progress over 3 weeks or longer

● Specific constellations of symptoms

○ typical​ - rapid onset, severe symptoms, productive cough, dense consolidation on CXR Don't forget about the age old question of What is the definition of premises?

○ Atypical​ - slower onset, nonproductive cough, patchy interstitial pattern on CXR ● environment in which pneumonia was acquired 

○ Community acquired- patient not recently (>14 days) in hospital or chronic care facility

○ Nosocomial - patient in a hospital at the time the infection developed

Five radiologic CXR patterns

1. Lobar pneumonia

2. Bronchopneumonia

3. Interstitial pneumonia

4. Lung abscesses

5. Nodular lesions

Pathogenesis of streptococcus pneumonia 

1. Thick outer layer capsule which block phagocystosis; type 3 has the thickest capsule 2. Immunoglobulins and complement are important opsonins that allow phagocytosis to ingest invading pneumococci

3. Step. pneumonia does not produce protease and seldom destroys lung parenchyma 4. It does not cross anatomic barriers such as lung fissures

5. Disease manifestations are caused primarily by the host’s inflammatory response Streptococcus pneumonia Prevalence and Predisposing factors 

1. S. pneumonia is the most common form of community-​ ​acquired​ ​bacterial​ ​pneumonia 2. Risk is higher in patients with deficiencies in opsonin production

a. Hypogammaglobulinemia, complement deficiency, HIV infection We also discuss several other topics like What is the meaning of crying?

3. Splenic dysfunction increases the risk of fatal pneumococcal bacteremia 4. Risk is increased in patients with chronic diseases

a. Cirrhosis, alcoholism, nephrotic syndrome, congestive heart failure, COPD Eye

Case study

sensation of a foreign body in left eye. Pain when blinking. Woke up one morning and eye was glued shut w/ yellow exudate-- eye was extremely red and sensitive to light after prying it open--- blurry vision outlined by halos. Large dendritic lesion that stained w/ fluorescein discovered w/ slit lamp @ ophthalmologist’s. This indicated herpes simplex keratitis. Disease:​ ​herpes simplex keratitis

Pathogen:​ ​HSV (typically type I)

Diagnostics:​ ​fluorescein stain, slit-lamp examination, corneal scrapings, gram stain, giesma stain

Treatment:​ ​antibiotics (broad coverage in pathogen unknown), topical fluroquinolones Clinical​ ​manifestations:​ ​(vary​ ​based​ ​on​ ​conditions)

1. Bacterial

a. Leading cause keratitis (65%-90% of cases)

b. Gram + organisms typically cultured (staph. A -- most common)

c. Most destructive - gram (-) pseudomonas aeruginosa

2. Viral

a. Recurrent red eye - HSV keratitis

i. Stresses induce reactivation

b. Foreign body sensation, dendritic lesions are typical symptoms

3. Fungal

a. Corneal ulcers caused by aspergillus most commonly follow an eye injury from organic materials

i. Candida can also cause ulcers (tend to me more indolent)

4. Protozoal

a. Rare but very serious causes of corneal ulcers

b. Acanthamoeba most commonly develop in contact lens wearers

Typical signs that will indicate eye infection

Key points - about keratitis (corneal infection)

- Condition needs to be treated quickly to prevent blindness

- Usually preceded by a break in the cornea

- Streptococcus pneumonia causes a well circumscribed ulcer w/ sharp margins - Pseudomonas aerguinosa is associated with hard contact lenses. It is very destructive and causes severe eye pain

- HSV causes distinct dendritic lesions that take up fluorescein. Consider this diagnosis in the hospitalized patient that develops unilateral red eye

- Aspergillus usually follows an eye injury from organic matter ( i.e. tree branch) - Acanrhamoeba occurs in contact lens wearers who use tap water with their cleaning solution


Case study

recurrent ear infections since age 12. Patient complained of severe left earache 3 days before being admitted to hospital-- ear drops were prescribed by local physician which helped the pain go away. The night before being admitted to the hospital patient complained of headache and being sort of disoriented. 1 hour after having headache patient began vomiting, and did so 5

times during the night. Morning of admission his wife said he appeared drowsy. He stayed home from work sleeping most of the morning . he awoke around noon but didnt recognize his wife. He spoke in incoherent sentences and became very restless. Around 4pm he failed to respond when his wife called his name so he was brought to the emergency room. Physical exam reported 40 C temp. Blood pressure 140/100, pulse 140 per minute, respiratory 20 per min. Man appeared very ill and only moved his limbs in response to pain. Patients ears were bilaterally blocked w/ cerumen. Pupils of his eyes were dialted 8mmm but reacted to light. Optic disk margins were flat. Neck was very stiff, w/ both Kernig’s and Brudzinski’s signs present. Coarse diffuse rhonchi were evident throughout all lung fields. No skin lesions were seen. Neurologic exam showed no cranial nerve abnormalities. Reflexes were symmetrical & patient moved all limbs. Labratory workup found peripheral WBC count of 19500/mm^3, w/ 39% polymorphonuclear luekocytes (PMNs), 50% bands forms, 6% lymphs, 5% monocytes. Hematocrit was 35.5% and chest X-ray (CXR) showed no infiltrates. A lumbar puncture was performed in the emergency room. Opening CSF pressure was found to be 560 mm H2O (normal: 70 to 180 mm). A CSF analysis showed a WBC count of 9500/mm3 (95%PMNs), protein 970 mg/dL (normal: 14 to 45 mg/dL) and glucose 25 mg/dL, with simultaneous serum glucose level 210 mg/dL (normal:50 to 75 mg/dL, generally two thirds of serum glucose). Gram-stain of the CSF revealed gram-positive lancet-shaped diplococci. Cultures of CSF and blood grew S. pneumoniae.

Disease:​ ​bacterial meningitis

Pathogen:​ ​streptococcus pneumonia

Symptoms:​ ​URT/ Ear infection, fever, headache, generalized pain, inflammation of meninges, stiff neck

diagnostics:​ lumbar puncture, gram stain, CT scan of head

Treatment:​ ​antibiotics (Penicillin + Vancomycin)

Key points - about clinical manifestations in bacterial meningitis

1. URT ot ear infection interrupted by the abrupt onset of meningeal symptoms a. Generalized, severe headache

b. Neck stiffness

c. Vomiting

d. Depression of mental status

2. Physical findings:

a. Brudzinksi’s (neck flexion) and kernig’s (staright leg raise) signs are insensitive; head jolt maneuver may have higher sensitivity

b. Abnormal ear exam

c. Petechial or purpuric skin lesions

d. Neurologic exam should look for focal findings (suggests a space - occupying lesion) and asseses mental status (glasgow score = important prognostic factor)


Case study

Increasing shortness of breath and ankle swelling. Had dental work done ~15 weeks before hospital admission. Experienced shortness of breath after any physical exertion following dental work. Increasing fatigue, night sweats, and intermittent low-grade fever. Diastolic murmur, II/VI was noted along the left sternal border, maximal at the third intercostal space was discovered. He was treated as an outpatient with diuretics for left-sided congestive heart failure (CHF). experienced increasingly severe shortness of breath and coughed up frothy pink phlegm. Temp was 39C blood pressure 106/66 mmHg pulse 85 per min, respiratory rate 36 per min. Diffuse wheezes and rales were heard in lower ⅔ of both lungs. Heart demonstrated loud S3 Gallop, II/VI nearly holosystolic murmur heard loudest in the left third intercostal space radiating to the apex, and an II/VI diastolic murmur heard best along left sternal border. Liver and spleen not palpable edema of the ankles extending midway up the thighs. Nail beds had no splinter hemorrhages.

Laboratory found WBC count of 11,700/mm^3, 69% polymorphonuclear leukocytes, 4% band forms, 22% lymphocytes, and 3% mononuclear cells, and a hematocrit of 30%, normochromic, normocytic. Urinalysis showed 1+ protein with 10-20 red blood cells and 5-10 white blood cells per high power field. Erythrocyte sedimentation rate was 67 mm/h. Electrocardiogram showed normal sinus rhythm, with left bundle branch block. Chest radiograph revealed extensive diffuse perihilar infiltration bilaterally. Four of four blood cultures were positive for S. viridans Disease:​ ​infective endocarditis

Pathogen:​ ​streptococcus Viridans

Symptoms:​ ​low-grade fever, chills, fatigue, anorexia, malaise, myalgias, lower back pain Diagnostics:​ ​blood culture, echocardiography (TEE), modified duke criteria Treatment:​ ​antibiotics

Key points -- About the causes of infective endocarditis

1. Native valve endocarditis

a. Most common cause is streptococcus:

i. S. Viridans is number one

ii. S. faecalis (eneterococcus)

iii. S. bovis (associated w/ colonic cancer)

b. Staphylococcus auereus is the second most common cause

c. HACEK group is an uncommon cause, but consider in culture- negative cases 2. Intravenous drug abusers

a. Most common cause is S. aureus

b. Gram (-) aerobic bacilli are the second most common cause (psuedomonas aerguinosa)

c. Fungi

d. Multiple organisms

3. Prosthetic valve

a. Early is the result of nosocomial pathogens

b. Late (more than 2 months post operation) is the result of mouth and skin flora

Key points -- About the physical findings in infective endocarditis

1. A cardiac murmur is heard in nearly all patients

a. Absence should call into question the diagnosis

b. Classic changing murmur is rare, but may occur with rupture of chordae tendinae c. New aortic regurgitation is the result on infective endocarditis until proven otherwise

2. Embolic phenomenon are found in up to 50% of all cases

a. Are most common in the conjunctiva; clusters can be found anywhere b. Splinter hemorrhages, linear streaks, are found under nails

c. Osler nodes, painful raised lesions in the pads of the fingers or toes, are evanescent

d. Janeway lesions, red macules, are most persistent and most common in acute endocarditis attributable to staphylococcus aureus

e. Roth spots are retinal hemorrhages with a clear center

3. Splenomegaly can be found; left upper quadrant tenderness can occur with embolic infarction

4. Check all pulses as a baseline b/c of the risk of obstructive emboli

5. Perform a thorough neurologic exam; a sudden embolic stroke can develop GIT

Case study

52 year old black woman with rheumatoid arthritis for 24 years was admitted to the hospital with complaints of fever and diarrhea for the preceding 24 hours. She was hospitalized a month earlier for neck surgery and received 10-day course of a broad spectrum antibiotic (ceftazidime). Antibiotic treatment was completed the day of discharge (18 days before her second admission) . she was doing well in rehab hospital until 3 days prior to admission, when she developed a fever to 38.9C associated with shaking chills and persistent severe watery diarrhea (25-30 bowel movements daily). One day before admission, she noted abdominal cramps, nausea, vomiting, and anorexia. The rehab nurse found the woman’s blood pressure to be 70/50 mmHg and referred her to the emergency room. Medications: aspirin and large quantities of antacids

Epidemiology​: her son had brought her an egg salad sandwich from famous deli, which they shared 16 hours before onset of the illness. Her son also has severe diarrhea. Physical​ ​examination:​ ​temp. 39C, blood pressure 70/50 mmHg, pulse rate of 120 per minute and respiratory rate 20 per minute. She was moderately ill appearing, with dry mucous

membranes and a dry, fissured tongue. Abdominal exam revealed hyperactive bowel sounds and mild diffuse tenderness, no skin lesions were seen.

Laboratory​ ​findings:​ ​WBC 7100/mm3, with 10% polymorphonuclear leukocytes (PMNs), 63% bands, 19% lymphocytes; blood urea nitrogen of 63 mg/dL; and serum creatinine of 2.1 mg/dL. Methylene blue smear of the stool: few PMNs and few mononuclear cells. Gram stain: mixed flora. Stool culture: salmonella enteritidis

Disease:​ ​diarrhea (gastroenteritis)

Pathogen:​ ​salmonella enteritidis

Symptoms:​ ​diarrhea, abdominal pain, bloody stool, enteric fever

Diagnostics:​ ​examination of stool (methylene blue stool), gram stain, culture of stool Treatment:​ ​antibiotics, fluid and electrolyte replacement -- most are self limiting

Key points - about Salmonella Gastroenteritis

1. Gram (-) bacillus, does not ferment lactose, motile

2. Attaches to intestinal and colonic cells, and injects proteins that stimulate internalization 3. Spreads to mesenteric nodes; salmonella choleraesuis and S. typhi often enter the bloodstream

4. The organism is acid-sensitive; risk factors for disease include

a. Antacid use

b. Prior antibiotics (reducing competition for normal flora)

c. Depressed immune system

5. Contracted from contaminated foods (prevalent during summer)

a. Chicken products

b. Contaminated processed foods

c. Infected pet turtles, rodents, iguanas, birds

d. Contaminated water supply (S. typhi)


Case study

A 23 year old white woman was admitted to the hospital with complaints of left flank painful for 4 days and fever for 2 days. One week before admission (4 weeks after her honeymoon), she noted mild burning on urination. Four days before admission, she noted left flank pain. Two days before admission, she experienced fever associated with rigors and increasingly severe flank pain. She gave a past medical history of recurrent UTI over the past 5 years, requiring antibiotic treatment once annually. She denied vaginal discharge and was completing her menstrual cycle.

Physical​ ​examination:​ ​blood pressure of 80/50 mmHg, a pulse of 125 per min. And her temp was 37.8C. She appeared very ill and in pain. Remainder of her physical exam was normal, except for mild left costovertebral angle tenderness. No suprapubic tenderness was elicited. Her pelvic exam was within normal limits.

Lab​ ​work:​ ​revealed a WBC of 10,200/mm3, with 81% PMNs and 2% bands; a hematocrit of 36%, a blood urea nirtrogen of 3mg/dL, and a serum creatinine of 0.4 mg/dL. Urinalysis showed a specific gravity of 1010 g/mL, a pH of 5, 100 WBCs per high-power field (normal: 0-5) and 0-2 red blood cells per high power field (normal). No protein or glucose was detected. A urine culture showed more than 105 E. coli, and 2 of 2 blood cultures grew E. coli Disease:​ ​UTI- cystitis

Pathogen:​ ​Escherichia coli

Symptoms:​ ​Dysuria, frequent urination, blood in urine

Diagnostics:​ ​urinalysis, unspun gram stain, urine culture, ultrasounds, intravenous pyelogram Treatment:​ ​antibiotics

Key points -- about clinical manifestations of UTI

1. Symptoms of cystitis and pyelonephritits overlap

2. Cystitis symptoms include dysuria, urinary frequency, hematuria, suprapubic discomfort 3. Pyelonephritits symptoms include fever and childs, and costovertebral angle pain and tenderness; the disease is more likely to occur in

a. Diabetic patients

b. Elderly patients

c. Patients who have had cystitis symptoms for more than 7 days

4. Asymptomatic bacteriuria is defined as a positive culture with no symptoms and usually w/o pyuria

a. Treat pregnant women to prevent low birth weight neonates

b. Treat adolescent children to prevent renal scarring

5. Urethritis can be mistaken for cystitis; usual indicators are fewer than 10^5 bacteria on culture and a lack of suprapubic tenderness

6. Vaginitis can mimic cystitis; pelvic exam is a must if symptoms associated with vaginal discharge


Case study

86 yr old white woman underwent cardiac catheterization 3 months before admission. Several days after her catherterization, she noted a fever that lasted 2-3 days. Approximately 3 weeks after her catheterization, she began experiencing dull pain in the lumbosacral region that progressively worsened over the next 2 months. Pain was not relieved by over-the counter pain medications and it became so severe that she sought medical attention in the emergency room. She reported a 25- pound (11.3 kg) weight loss over the 3 months

Physical​ ​examination:​ temp was 36.4C. Pulse = 84 per min. General appearance was that of an elderly woman complaining of back pain. A 2/6 systolic ejection murmur was noted along the left sternal border. Palpation over the L-S spine area elicited moderate tenderness. Motor and sensory exams of the lower extremities were within normal limits

Lab​ ​results:​ ​erythrocyte sedimentation rate (ESR) of 119 mm/h; white blood cell WBC count of 8.1/mm3, with 52% polymorphonuclear leukocytes (PMNs), 12.8% lymphocytes, and 10.8% monocytes; and a platelet count of 537,000/ mm3. A computed tomography (CT) scan showed marked decalcification of the L4-L5 vertebral bodies, with a “moth-eaten” appearance of the vertebral endplate in L5. a CT-guided aspirate grew no pathogens, but a repeat aspirate demonstrated an acute inflammatory reaction, with the culture was positive for S. aureus, two blood cultures showed no growth.

Disease:​ Osteomyelitis

Pathogen:​ ​staphylococcus aureus

Symptoms:​ ​localized back pain/tenderness, fever

Diagnostics:​ ​Xray, CT scan, MRI

Treatment:​ ​antibiotics (methicillin-sensitive)

Key points -- about the classification of osteomyelitis

1. Acute osteomyelitis develops over days to weeks

2. Chronic osteomyelitis develops over weeks to months and can persist for years 3. Hematogenous osteomyelitis occurs in children and elderly individuals 4. Infections at contiguous sites can spread to bone. Initial infections are the result of

traumatic injury, penetrating injury, orthopedic surgery, or diabetic or other forms of ischemic or neuropathic ulcer

Key points - about the pathogenesis, microbiology, and clinical manifestation of hematogenous osteomyelitis

1. Bacteria are trapped in small end vessels

a. At the metaphysis of long one in children

b. In vertebral bodies in the elderly; can also spread via batson’s venous plexus 2. Microbiology reflects the cause of bacteremia:

a. Neonates - E. coli, Staph. A

b. Adults - Staph. A

c. Elderly - gram (-) organisms, Staph. A

d. Intravenous drug users - pseudomonas aerguinosa

3. Clinical manifestations

a. Long bones - fever, chills, and malaise, plus soft tissue and swelling and pain (children)

b. Vertebral osteomyelitis - back pain and localized tenderness, plus high erythrocyte sedimentation rate or C-reactive protein


Case study

63 year old black man presented to the emergency room with a 1-day history of mild swelling of his right foot and ankle that was extremely tender to palpation. He had a long history of alcohol abuse and a history of cirrhosis. He was afebrile at the time of presentation and was sent home

with oral keflex. Two days later, he returned complaining of fever and increased swelling. He was admitted to the hospital and intravenous clindamycin and gentamicin were started Despite new therapy, his leg swelling and erythema failed to improve.

physical​ ​exam:​ ​appeared severely ill and septic. Temp. was 39.6 C, pulse was 120 beats per min. And blood pressure was 90/70 mmHg. Marked erythema was observed, along w/ edema of the right ankle that extended up the front and lateral regions of the leg, half way to the knee. A new 11 cm patch of dark reddish- purple skin was noted that was exquisitely tender to touch. No lymphadenopathy was observed.

Lab​ ​results:​ ​WBC count of 25,000, with 90% PMNs. an emergency surgical exploration revealed an area of necrotic fascia consistent with necrotizing fasciitis. Intraoperative cultures grew E. coli and bacteroides fragilis

Disease:​ ​nectrotizing fasciitis

Pathogen:​ ​E. Coli & Bacteriodes fragilis

Symptoms:​ ​fever, swelling, erythema, unexplained pain that increases rapidly Diagnostics:​ ​biopsy, surgical exploration; less used = Xray, CT, MRI

Treatment:​ ​surgery (and surgical debridement), antibiotics, additional measures (massive amounts of intravenous fluids)

Key points -- about necrotizing fasciitis

1. Deep subcutaneous infection causes necrosis of the fascia and subcutaneous fat 2. Causes include group A streptococci, community- acquired methicillin resistant staphylococcus aureus, or mixed infection with gram negative aerobes/anaerobes 3. Severe pain is often the earliest symptom; septic appearance and tachycardia are also suggestive

4. Surgical exploration or punch biopsy are required for diagnosis

5. Treatment must include:

a. Aggressive and often repeated surgical debridment

b. Systemic antibiotics

c. Volume replacement and vasopressors

d. For seriously ill patients -- intravenous administration of immunoglobulins should be considered


Case study

A married couple was sailing in the caribbean near jamaica with their three children. They livede primarily on their boat, but took several day trips to small island off the coast of jamaica. They noted some mosquito bites and ate some fruit while on the island. The man and the woman both suddenly came down with fever, chills, muscle aches, and loss of appetite. About 3 days into the illness, the man became jaundiced and began passing dark urine. The family sought treatment from a local jamaican physician, who diagnosed hepatitis secondary to ingestion of a toxic food. Two days later, the man became comatose and died.

The woman was referred to the university hospital for possible liver transplant. On further questioning, the medical staff learned that none of the children were sick despite eating the same diet. The family had begun a course of malaria prophylaxis. However, the parents had developed side effects from the chloroquine and had discounted prophylaxis 2 weeks before the onset of their illness.

Thin smears of the woman’s blood revealed many signet-ring trophozoites, with a parasitemia level estimaed to be 10%. She was treated with intravenous quinine and rapidly improved. In retrospect, her husband was determined to have died of untreated blackwater fever. Disease:​ ​malaria

Pathogen:​ ​plasmodium falciparum

Symptoms:​ fever, shaking, chills, loss of appetite, vague pains, headache, nausea, sweating Diagnostics:​ ​giesma stain, ELISA, PCR

Treatment:​ ​prophylaxis, aminoquinolones (chloroquine)

Key points - about genetics and other factors that affect susceptibility to malaria 1. Surface proteins on RBCs

a. Individuals negative for the Duffy blood group antigen are resistant to P. vivax b. Complement receptor 1 mutations reduce the severity of P. falciparum infection 2. Cytoskeleton defects in RBCs are protective

a. Heredity ovalocytosis, elliptocytosis, spherocytosis

3. Hemaglobinopathies confer resistance:

a. Sickle cell disease and sickle cell trait are resistant to P. falciparum

b. Other hemoglobin mutations and fetal hemoglobin are also resistant to P. falciparum

4. Low-level immunity increases the risk for severe disease:

a. Population immunity wanes in areas with low attack rates

b. Tourists lack immunity

c. In pregnant women, the placenta is affected, resulting in low birth weight infants Key points - about clinical presentation in Plasmodium infection

1. Patient presents with an influenza-like syndrome

2. Patient presents with jaundice

3. Presents with confusion or obtundation (less​ ​than​ ​full​ ​alertness) 


Case study

7 year old girl arrived in the emergency room in oklahoma with 2 day history of fever (39.8C), malaise, abdominal pain, nausea, and vomiting. She was discharged with a diagnosis of viral gatroenteritis. Four days later, she was seen at a second emergency room with persistent fever, anorexia, irritability, photophobia, cough, diffuse myalgia, nausea, and vomiting.

On physical exam, she was noted to have hepatosplenomegaly and an erythromatous popular rash with scattered petechiae on the trunk, arms, legs, palms, and soles. Lab​ ​findings:​ ​elevated WBC of 11,400/mm3, a low platelet count of 19,000/mm3, and elevated liver enzymes (AST: 279 IU/L; ALT: 77 IU/L). Intravenous doxycycline was initiated to treat suspected RMSF, and she was placed in intensive care. Her mental status declined, and she developed metabolic acidosis and respiratory failure, dying 6 days after her first visit to the emergency room.

A serum sample drawn 2 days before her death revealed 1:128 IgG anti- R. rickettsii antibody titer. Spotted-fever group rickettsiae were detected by immune-histo-chemical staining of autopsy specimens from brain, skin, heart, lung, spleen, and kidney. On questioning, the parents reported that their child played frequently in grassy areas near their home. They did not note any recent tick bite, but ticks had been frequently observed on the family’s pet dogs and often were manually removed by members of the household.

Disease:​ ​rocky mountain spotted fever

Pathogen:​ ​Rickettsia rickettsii

Symptoms:​ ​rash, fever, headache, malaise, myalgias, nausea, abdominal pain Diagnostics:​ ​epidemiology, clinical manifestations

Treatment:​ ​antibiotic therapy (Doxycycline)

Key points - about the clinical manifestations of RMSF

1. Incubation period is 2-14 days

2. Acute onset of nonspecific symptoms

3. Rash on ankles and wrists that spreads to trunk (spottless infection in 10%) 4. Other symptoms: aseptic meningitis, conjunctivitis, hemorrhages, respiratory distress syndrome

5. Deaths within 8-15 days if treatment not initiated in 5 days

Adult viral

Case study

An 18 year old college freshman presented to the student health office with fever and sore throat for 1 week. His temp. Was 38.9C, his tonsils were enlarged, and he had diffuse nontender lymphadeonpathy. The possibility of mononucleosis was raised, and itters for viral capsid antigen (VCA), IgG, and IgM were 1:20 and 1:80 respectively at that time. Over the next week, he became increasingly ill, developing scleral icterus and fever to 40.6 C Physical​ ​exam:​ ​tender, enlarged liver and palpable spleen. Multiple petechia were noted on both lower legs.

Laboratory:​ ​elevated liver transminases: 550 IU/L aspartate aminotransferase, 1000 IU/L alanine transaminase, 4000 IU/L lactate dehyrdogenase (LDH), and bilirubin 6.0 mg/dL (total) and 4.8 mg/dL (direct). His hematocrit was 25% and his white blood cell (WBC) count was 860/mm3, with 3% polymorphonuclear luekocytes (PMNs), 19% bands, 70% lymphocytes, and 10% monocytes. Numerous atypical lymphocytes were seen on smear. Platelets measured

23,000/mm3, and his erythrocyte sedimentation rate was 12mm/h. Repeat serology revealed a VCA IgM of 1L160 and VCA IgG of 1:640. Glucocorticoid therapy was considered; however, over the next 2 weeks, the fever spontaneously resolved, liver function tests returned to normal, hematocrit increased to 35%, WBC count improved to 3000/mm3 (with 70% PMNs) and platelets rose to 100,000/mm3. The young man’s spleen remained enlarged, and he was warned to avoid contact sports for the next few months

Disease:​ ​mononucleosis

Pathogen:​ ​epstein- barr virus

Symptoms:​ ​fever, sore throat, malaise, lymphadenopathy, splenomegaly Diagnostics:​ ​clinical suspicion confirmed by lab testing; monospot test, heterophil Ab agglutination, PCR

Treatment:​ ​cancer chemotherapy, radiation therapy, antivirals

Key points -- about the epidemiology, pathogenesis, and clinical manifestations of EBV 1. Spread by oral secretions, with 95% of adults carrying the virus

2. Infects B cells, and illness manifestations are the result of vigorous T cell and natural killer (NK) cell inflammatory response

3. Fever, sore throat, and lymphadenopathy are the classic triad of mononucleosis 4. Acute complications of the infection include splenic rupture, neurologic syndromes, and airway obstruction

5. Complications include hairy leukoplakia, B cell/ NK cell lymphoma, and leiomyosarcoma

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