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MICRO CASE-BASED SMALL GROUP DISCUSSION
SESSION 28
HIV
TUESDAY, APRIL 17, 2001
10:30AM – 12:30PM
READING ASSIGNMENT:
SHERRIS MEDICAL MICROBIOLOGY, CHAP. 50, PP. 619-622;
CHAP. 52, PP. 655-658;
CHAP. 41, PP. 547-555.
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Case 1
History. A 47 year-old woman presented with chief complaint of fever to 103 ºF,
non-productive cough and dyspnea which has progressed over one week. She was tested
HIV-positive 5 years ago at which time her CD4 lymphocyte count was 583. Zidovudine was
started, but she stopped taking it after one month and did not return to her doctor for follow-up.
She has anorexia and lost 70 pounds over the last 3 months.
She used heroin and cocaine intravenously for a six month period 6 years ago. She does not
smoke or drink, has no past STD's and is not sexually active. She has no known drug allergies
(NKDA).
Physical Examination. She was pale, diaphoretic and in acute respiratory distress. T 37.4º C, P
96/'min, R 30/min, BP 110/70. Oral thrush was present. Examination of the lungs disclosed
poor inspiratory effort and bibasilar crackles 2/3 of the way up the posterior lung field. She had
a tachycardia but no murmurs. Her abdomen was nontender, and there was no enlargement of
the liver or spleen. Pelvic exam was normal except for vaginal candidiasis. Neurologic
examination was normal.
Laboratory Evaluations:
Hgb
WBC
Segs
Lymphs
Monos
Eos
Basos
Platelets
ABG
CD4
HIV RNA level
Induced sputum
10.8 g/dl
7,500/mm3
43
41
9
6
1
248k/mm3
7.48(pH)/32(pCO2)/51(pO2)/23(HCO3)
%=11.#=235/mm3
234,000 copies/ml
Direct fluorescence positive for Pneumocystis carinii
1. What is Pneumocystis?
Pneumocystis carinii is an organism of uncertain taxonomic position with ribosomal RNA
sequences of fungi but DNA content, absent fungal protein elongation factor EF-3, and
antimicrobial susceptibility characteristics all suggestive of protozoa. Its life cycle
resembles sporozoa (protozoa). Similar (?identical) organisms are found in lungs of lower
animals. It is a cause of serious pulmonary infections almost exclusively in
immunocompromised humans.
2. How is Pneumocystis carinii acquired? Was this patient recently infected?
Study of epidemics suggest that person to person spread by airborne droplets occurs. Most
cases in the US including those in AIDS patients are thought to represent reactivation of
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latent infection. Nursery outbreaks in post-WWII Europe and more recently in Southeast
Asia as well as reports of increased numbers of secondary cases on oncology wards in the
US suggest person to person spread still occurs.
3. What is the mechanism by which Pneumocystis carinii causes pneumonia?
Pneumonia occurs in persons with suppressed T lymphocyte function as might be seen with
starvation, corticosteroid administration or in HIV infection when CD4 T-lymphocyte
count has dropped below 200/mM3. Virulence factors have not been identified. Pneumonia
is characterized by alveoli filled with desquamated alveolar cells, monocytes, organisms
and fluid producing a distinctive foamy appearance.
Type II pneumocytes are present. Round cells may be increased in the widened septa.
Healing is generally complete but some fibrosis and even residual thin-walled cavities may
be left.
4. How is infection with Pneumocystis carinii diagnosed?
Organisms can be identified morphologically in tissue biopsy or in pulmonary secretions.
Induced sputum, bronchoalveolar lavage (obtained with bronchoscope) have reasonable
yield. Organisms can be stained with Geimsa (trophozoite) or Gomori methenamine silver
(cyst). A fluorescent tagged anti-pneumocystis monoclonal antibody direct fluorescence
test is very useful.
The patient is started on intravenous trimethoprim/sulfamethoxazole (20 mg/kg/D trimethoprim:
100 mg/kg/D sulfamethoxazole) plus prednisone 40 mg twice daily. Two days later she is
improved: respiratory rate is down to 18/min, O2 saturation is 98% with FiO2 of 21%.
Trimethoprim sulfamethoxazole therapy is changed to oral. On day 5, she develops fever, a
morbilliform rash and elevations of AST, ALT and alkaline phosphatase.
5. To what can we attribute the rash? Are the rash, fever and abnormalities in liver function
related?
Rash, fever and hepatitis are characteristic of reaction to trimethoprim/sulfamethoxazole.
6. What alternative therapies are available?
Alternative treatments include pentamidine, trimetrexate, a dihydrofolate reductase
inhibitor, atovaquone, a hydroxynapthoquinone, or the combination of primaquine and
clindamycin can all be used. Seriously ill patients as indicated by a large a-A gradient
benefit from systemic corticosteroids. In patients with moderate to severe pneumonia,
pentamidine should probably be the first alternative.
7. What is the likelihood of an adverse reaction to trimethoprim sulfamethoxazole in a patient
with AIDS?
Over 50%.
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8. Can relapses of pneumonia due to Pneumocystis carinii be prevented? How?
Yes, prophylactic low dose T/S or dapsone or aerosolized pentamidine will reduce the
frequency or prevent recurrences.
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Case 2
A 29 year-old woman with AIDS was admitted with fever, profuse watery diarrhea and right
upper quadrant abdominal pain for 23 days. outpatient stool evaluation disclosed
Cryptosporidium parvum but no WBC's. Paromomycin and anti-diarrheal agents failed to stop
the diarrhea. She had no tenesmus and denied blood in the stools. She felt warm but did not take
her temperature.
Her past history includes HIV infection diagnosed 3 years ago. Oral candidiasis was diagnosed
last year. She is single and lives with her mother and 9 year old daughter. She is actively using
heroin and cocaine.
Physical Examination. She appeared weak and emaciated but in no acute distress.
T 37.10C, P 120/min, R 24/min, BP 90/50 supine.
Head, eyes, ears, nose and mouth were normal. There was no cervical adenopathy. Lungs were
clear to percussion and auscultation. There were increased bowel sounds and mild diffuse
abdominal tenderness most prominent in the right upper quadrant. The rectum was unremarkable
and stool guaiac was negative. Extremities and neurological examinations were normal.
Laboratory Evaluations:
Hgb
WBC
Segs
Lymphs
Monos
Platelets
Na
K
Cl
CO2
Creatinine
X-rays of chest and abdomen
12.0
2,900
66
15
18
203k/mm3
133 meq/L
3.3 meq/L
107 meq/L
14 meq/L
2.3 mg/dl
normal
In the hospital hyperalimentation was started. Octreotide plus azithromycin were started without
effect.
Colonoscopy and EGD showed cryptosporidia on the colonic mucosa and in the area of the
ampulla.. AFB blood cultures grew Mycobacterium avium complex and she was started on
clarithromycin and ethambutol.
1. What is Cryptosporidia? Describe its life cycle.
Cryptosporidia are sporozoan protozoan parasites that infect the intestinal tract of a wide
range of mammals including humans. Life Cycle. The fully mature, infective oocysts are
excreted in the stool of the parasitized animal. Following ingestion by another animal,
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sporozoites are released from the oocyst and attach to the microvilli of the small bowel
epithelial cells where they are transformed into trophozoites. They divide asexually by
multiple fission (schizogony) to form schizonts containing eight daughter cells known as
type 1 merozoites. Upon release from the schizont, each daughter cell attaches
itself to another epithelial cell, where it repeats the schizogony cycle, producing another
generation of type I merozoites. Eventually, schizonts containing four type 2 merozoites are
seen. Incapable of continued asexual reproduction, these develop into male (microgamete)
and female (macrogamete) sexual forms. Following fertilization, the resulting zygote
develops into an oocyst that is shed into the lumen of the bowel. The majority possess a
thick protective cell wall that ensures their intact passage in the feces and survival in the
external environment. Approximately 20% fail to develop the thick wall. The cell
membrane ruptures releasing infective sporozoites into the intestinal lumen and initiating a
new "autoinfective" cycle within the original host. In the normal host, acquired immunity
dampens both the cyclic production of type 1 merozoites and the formation of thin walled
oocysts, halting further parasite multiplication and terminating the acute infection. In the
immunocompromised (AIDS) both processes continue resulting in chronic infection.
2. How is cryptosporidia acquired?
Domestic animals are the major reservoir in this country. Transmission occurs by person
to person, animal to person, and from the environment, particularly water. The principle
route of transmission is by direct fecal-oral spread. Waterborne outbreaks, including one
in Milwaukee affecting 403,000 persons, have occurred.
3. How does cryptosporidia cause disease?
Organisms apear as spherical structures arranged in rows along the microvilli of epithelial
cells. They are covered by a double membrane derived from reflection, fusion and
attenuation of the microvilli and are thus considered intracellular. There may be villous
atrophy and blunting, crypt hyperplasia and lengthening, and infiltration of the lamina
propria with inflammatory cells. Mechanism of diarrhea is not known. Studies in AIDS
patients have shown secretory mechanisms unaffected by fasting and malabsorptive
mechanisms with positive D-xylose and decreased absorption of vitamin B12 as well as
steatorrhea.
4. How is it treated?
There is no palliative or curative treatment for cryptosporidiosis. The disease is selflimited in the immunocompetent. Currently paromomycin (a luminal antimicrobic) or
azithromycin to treat infection or octreotide (a somatostatin analogue) to control the
diarrhea are used in persons with AIDS. Bovine transfer factor and hyperimmune bovine
colostrum have been experimentally shown to ameliorate the symptoms. Recent
publications have documented clinical resolution of cryptosporidiosis in patients who
responded to highly active antiretroviral therapy.
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5. What is Mycobacterium avium complex (MAC)?
Mycobacterium avium complex is a group of related acid-fast organisms that grow only
slightly faster than M. tuberculosis and can be divided into a number of serotypes. Some
cause disease in birds; others cause disease in mammals but not birds. They are found in
soil and water and in infected animals.
6. Describe the pathogenesis of infection with MAC in persons infected with HIV.
Asymptomatic colonization after ingestion or inhalation precedes infection. Symptomatic
localized infection can occur either in the lung or the G1 tract. The GI tract is probably the
most common portal of entry. Focal pneumonias are uncommon in AIDS and
dissemination usually ensues. Localized GI infection can occur from esophagus to rectum
but the duodenum is most common. Dissemination usually involves many organs-- most
commonly the blood, bone marrow, liver, spleen. and lymph nodes; but the organism has
been recovered from the eye, brain, meninges, CSF. skin, tongue. heart, lung, stomach,
thyroid, breast, parathyroid, adrenals, kidney, pancreas, prostate, testis and urine.
Microscopically, tissues are filled with large numbers of distended histiocytes that on
Ziehl-Neelson staining are packed with acid-fast bacilli. The histologic picture in
disseminated MAC disease is similar to that seen in lepromatous leprosy and reflects an
inability of the host to mount an efftective cell-mediated immune response which would be
manifest as a granulomatous reaction. Phagocytosis by macrophages in patients with AIDS
appears to be intact but intracellular killing does not occur.
7. What are the clinical manifestations of infection with MAC in persons with AIDS?
Fever and weight loss are characteristic with chronic diarrhea, abdominal pain and signs of
extrahepatic biliary obstruction occurring less commonly. Severe anemia is common.
Rarely reported are localized pneumonia, endobronchial lesions, arthritis, skin lesions and
endophthalmitis.
8. How is infection with MAC diagnosed? What specimens are useful for culture?
Diagnosis is established by recovery of the organism from a normally sterile site but blood,
bone marrow, lymph node, and liver are most common. Blood cultures are set up in
specialized liquid medium with radiometric detection systems developed specifically for
mycobacteria. DNA probes are used to rapidly identify any growth of acid- fast- positive
organisms. Tissue samples show infiltration with swollen macrophages containing large
numbers of mycobacteria on acid-fast staining.
9. Is infection with MAC treatable? What medications are used in its treatment? For
prevention?
Yes, initial antimicrobial treatment should be with clarithromycin (high dose) or
azithromycin plus ethambutol. Additional drugs may be used but recent results of clinical
trials have shown that addition of clofazimine to a two drug regimen containing one of the
macrolides plus ethambutol provided no benefit.
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Besides clofazimine, amikacin , rifampin, rifabutin ciprofloxacin can all be used. AT
LEAST TWO DRUGS SHOULD BE USED TO PREVENT EMERGENCE OF
RESISTANT MUTANTS. Clinical response may require 2 - 8 weeks and therapy should
be continued for life. PREVENTIVE THERAPY in patients at high risk (T-cell counts <50
-100) with rifabutin or clarithromycin or azithromycin being recommended for lifelong
prophylaxis.
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Case 3
A 43 year-old physician presents to your office because his HIV test was positive two months
previously, at the time of a life insurance evaluation. As a result of the test he revealed his
bisexual life experiences to his wife, also a physician, who decided to leave the marriage with the
5 year-old daughter and 3 year-old son. The patient denied fever, any pain, skin problems,
diarrhea or weakness. He admitted to anorexia, a 12 pound weight loss over two months and
insomnia.
Past history: positive PPD since age 5 and oral HSV since childhood with about 3 recurrences
per year. He is on no medications and has no known drug allergies (NKDA).
Physical examination. He is depressed appearing but in no physical distress.
T 36.90C, P 84/min, R 18/min BP 122/80 Wt 87.3 Kg
Examination was normal other than a 1 cm. R supraclavicular and a 0.5 cm L posterior cervical
lymph node.
Laboratory evaluations (brought by patient)
CBC
normal
Liver function tests
normal
Creatinine
0.9 mg/dl
1. What test(s) would you order to assess the stage of his HIV infection?
CD4+ percentage of lymphocytes and total CD4+ cell counts. In addition quantitative
assessment of HIV RNA in plasma provides prognostic information at the time of
presentation which adds to the information obtained with CD4+ cell count. Independent of
CD+ lymphocvte percentage or count, the greater the amount of HIV RNA the more
rapidly the disease will progress.
2. What would you tell him about his future sexual experiences?
He should avoid sexual activitv in which there is opportunity for exchange of body fluids.
That includes heterosexual intercourse, oral sex. and anal sex which is particularly risky. If
he is unable to abstain he should: 1. ALWAYS use a condom in situations in which body
fluids might be exchanged and 2. Strive to establish mutually monogamous relationship.
3. Would you offer to refer him for psychiatric counseling?
In addition to recently receiving the diagnosis of HIV-positive, this doctor's wife left with
his two children. He is described as anorexic, lost 12 pounds and can't sleep-all symptoms
of depression. Either his depression must be dealt with by the primary physician with
counseling and probably medication OR he should be referred to a qualified mental health
professional.
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He returns two weeks later. He admits to feeling depressed; he misses his children; and he still
has insomnia. His appetite is improved; his weight is unchanged. He has an appointment with a
psychiatrist on the following day. Both of you review the laboratory results.
HIV
PPD
Anti HBs
Toxoplasmosis titer
CD4+ lymphocyte count
HIV RNA level
ELISA and WB positive
negative
positive
positive
% 24, = 306/mm3
8400 copies/ml
4. Explain the significance of each of the above tests.
1. HIV status is confirmed positive.
2. PPD now negative. He is probably anergic.
3. He has antibody to Hepatitis B surface antigen. He is immune and does not have chronic
hepatitis B. He will derive no benefit from Hepatitis B Vaccine.
4. He is at risk for toxoplasmosis encephalitis in the future and may benefit from
prophylaxis.
5. The CD4+ count is low but not in the AIDS range.
6. With a CD4 + count of 306 and viral load of 8400, he is in the second prognostic quartile
with an 65% estimated likelihood of developing AIDS in 9 years. (See attached table at
end of facilitator guide).
5. Would you recommend antiretroviral therapy" Would you use one antiretroviral drug or
multidrug therapy?
Most experts would start combination therapy at this stage even though he has never been
treated. Combinations include zidovudine (ZDV) or stavudine (D4T) plus lamivudine
(3TC) plus a protease inhibitor (indinavir or nelfinavir) or a non nucleoside reverse
transcriptase inhibitor (nevirapine). Other nucleosides, (didanosine. zalcitibine), NNRTI's
(delavridine) and protease inhibitors (saquinavir, ritonavir) can be used either to substitute
for intolerance or as part of salvage regimens. Patients must be active participants in
treatment decisions. Education of the patient about schedule, drug and food interactions
and THE ABSOLU'TE NECESSITY FOR COMPLIANCE is a requirement and ample
time should be alloted.
6. What are the side effects of zidovudine? List one major side effect of didanosine, lamivudine,
zalcitabine, stavudine, saquinavir, riconavir, and indinavir.
MAJOR TOXICITIES ONLY
Zidovudine - Bone marrow suppression neutropenia and anemia which is more severe in
late stage HIV disease. Can monitor compliance with macrocytosis.
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Myopathy - less common but seen in late stage disease and long term therapy.
Lactic acidosis associated with mitochondrial toxicity in the liver - RARE
Nuisance side effects: Nausea, vomiting and headache
Didanosine - Pancreatitis - 5-9%
Peripheral neuropathv (burning or numbness in distal extremities) - 5-12%
Nuisance: Nausea, vomiting, diarrhea
Lamivudine-Almost none! (nausea, diarrhea and abdominal pain)
Zalcitibine - Neuropathy, pancreatitis, mouth or throat sores
Stavudine - Neuropathy, nausea, headaches, diarrhea
Saquinavir- Nausea. diarrhea, abdominal pain. headache
Ritonavir - Nausea, vomiting, peripheral and circumoral neuropathy
Indinavir - Diarrhea, Nephrolithiasis
Nelfinavir- Diarrhea, rash
7. Should he receive prophylactic therapy to prevent Pneumocystis carinii pneumonia?
No.
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Case 4
A 26 year-old woman with known HIV infection is admitted at 39 weeks gestation in active
labor. She was initially diagnosed as having HIV infection by her obstetrician at her first
prenatal visit at 16 weeks’ gestation when she admitted that she had used intravenous drugs in
the past. She did not return for follow up visits. Her pregnancy has been otherwise
unremarkable. She has been on no medications. Her infant weighted 3400 g. and had APGARS
of 9 at one minute and 10 at 5 minutes. He was a vigorous baby and the physical examination
was entirely normal.
1. What is the likelihood that the infant acquired HIV infection from his mother?
The risk of mother-to-child transmission of HIV ranges from about 15 to 35 percent. The
lowest rates are reported in Europe. the highest in Africa. Transmission is influenced by
multiple factors. An important determinant may be viral load. The presence of p24
antigenemia has consistently been associated with increased transmission. Other factors
associated with increased transmission include low maternal CD4 cell counts. advanced
HIV disease and increased levels of beta., microglobulin. Biologic and genetic variation of
HIV mav also influence the risk of transmission. e.g., it has been suggested by some that
syncytium-inducing virus, which is associated with advance clinical disease, may be more
efficiently transmitted than non-syncytium-inducing virus. High levels of maternal
neutralizing- antibody have been shown to be associated with reduced transmission in some
studies. Other risk factors for mother-to-child transmission include chorioamnionitis and
sexually transmitted diseases. Mode of delivery, duration of labor, interval from time of
membrane rupture to delivery and events during labor and delivery that can expose the
infant to the mother's blood (e.g., episiotomy, severe lacerations) may also be important.
2. How is the virus transmitted from mother to infant?
There is evidence from examinations of placental and fetal tissues that HIV infection can
occur in utero. Indirect evidence suggests that a substantial proportion of infants acquire
the infection during the peripartum period. HIV is present in breast milk and infants may
also acquire infection through breast feeding.
3. What is known about the pathogenesis of the infection in the fetus infant?
The HIV infects the CD4+ subset of T lymphocvtes in addition to other cell types.
Infection of helper T cells causes abnormalities of lymphocyte function. syncytium
formation and cell death. Because the CD4+ lymphocyte plays a key role in many arms of
the immune svstem. including B cell function and suppressor T cell function. the resultant
helper T cell lymphopenia and lymphocyte dysfunction produce the many immunologic
defects that form the basis for the clinical manifestations of AIDS.
The infection of a cell begins with the attachment of the HIV envelope glycoprotein to the
cell’s CD4 molecule, which serves as the HIV receptor. Co-receptors include the chemokine
receptors and mediate attachment of monocytotropic (CCR5) and T-lymphocytotropic
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(CCXCR4) types of HIV. The virus then fuses with the cell membrane, enters the cell, and
becomes uncoated within the cytoplasm. After transcription of the viral RNA into DNA by
the reverse transcriptase enzyme of the virus, the DNA is circulated, and some of it is
integrated into the host cell DNA in latent proviral form. On activation, the proviral DNA
is transcribed to RNA; then this RNA is translated so that the HIV proteins are
synthesized. The infection is characterized bv high level replication in lymphoid cells and
low level replication or even latency in other lymphoid cells or macrophages. Rate of
progression is determined by both viral and host factors.
Abnormalities of the immune system: Absolute lymphopenia is common in adults with
AIDS but appears to be less common in children. In BIV-infected children, defects in B cell
function are usually apparent earlier than those of cell-mediated immunity, and recurrent
or serious bacterial infections are the result. Both B cell abnormalities and deficient helper
T lymphocyte function contribute to defective humoral immunity. Despite abnormal B cell
function, elevated serum immunoglobulin levels are a hallmark of HIV infection in
children. Other abnormalities seen in children with HIV infection include diminished
interferon and interleukin-2 production as well as abnormal natural killer cell activity.
4. How is the viral infection detected in the infant?
The diagnosis of HIV infection in infants born to HIV-infected mothers is made after the
detection of the virus in culture, the HIV genome by the polymerase chain reaction, the
viral antigen, or the persistence of HIV antibody beyond the age of 18 months. The
sensitivity of viral culture and PCR is only about 40% at birth. However, after one month,
the sensitivity of viral culture is about 90%, and the sensitivity of PCR is probably even
higher. The presence of HIV antibody before 18 months of age may represent HIV
infection in the infant or just passive transfer of maternal antibody.
5. Is prevention from mother to infant possible?
In a randomized. placebo-controlled trial, investigators found that in pregnant women
with CD4 counts greater than 200 per cubic millimeter and no previous antiretroviral
drug treatment, a regimen of antepartum and intrapartum zidovudine for the mother and
6 weeks of zidovudine for the newborn reduced the risk of transmission by about two
thirds from 25.5% to 8.3%. Current trials employing combination antiretroviral therapy
in pregnant women and their infants are ongoing. Other approaches to reducing the
transmission HIV from mother to child include avoidance of breast feeding and reduction
in peripartum exposure (eg, avoidance of intrapartum invasive procedures, vaginal
disinfection, aggressive treatment of sexually transmitted diseases. ??cesarean section).
6. What are the long-term consequences of the infection in the infant?
HIV-related symptoms and signs are rarely present at birth but develop over subsequent
months or years. In about a quarter of infected children, HIV infection progresses rapidly
to AIDS or death in the first year. In the remainder, it progresses more slowly, with some
children surviving beyond childhood years. The proportion of infected individuals who
have rapid progression of disease is higher in children than adults. This may be explained
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by the immaturity of the immune system at the time of HIV acquisition, the infecting dose
of virus, and the route of infection.
Pneumocystis carinii pneumonia has a peak incidence between 3 and 6 months of age and is
associated with a high mortality rate. Neurologic manifestations are common in children
with rapidly progressive disease, typically with manifestations developing in the second six
months of life. Recurrent bacterial infections and lymphocytic intestitial pneumonitis are
important manifestations in children. Problems with growth and pubertal development are
observed among children entering adolescence.
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Case 1:
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Slides 1 and 2 are chest x-rays from the patient which depict early and late
Pneumocysris carinii pneumonia. The first shows early interstitial changes esp. on
the left. The second shows left lower lobe consolidation with air bronchograms
during the time when she was quite hypoxemic.
Slide 3 is an H. & E. stain of lung with PCP. Alveoli are filled with acellular,
amorphous appearing proteinaceous material.
Slide 4 through 6 are methenamine silver stained sections of lung showing the cysts
at progressively higher magnification. The last shows both the comma (side view)
and saucer appearance of the cysts.
Slide 7 is a sputum specimen stained with fluorescein conjugated monoconal antipneumocystis antibody.
Case 2:
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Slides 8 and 9 are AFB stains of preserved stool with cryptosporidia oocysts.
Slide 10 is a preserved stool specimen stained with fluorescein conjugated anticryptosporidia antibody.
Slides 11 and 12 are small bowel biopsies from a patient with cryptosporidiosis.
Slides 11 shows fairly normal appearing villi with increased inflammation in the
lamina propria and tiny organisms on the surface. Slide 12 is a high power of the
organisms on the villus surface.
Slides 13 through 15 are CT scans through the abdomen. Slide 13 is a normal study.
Slide 14 shows massive bowel wall edema secondary to infiltration of the bowel wall
with Mycobacterium avium complex organisms (Correlate with slides 16 and 17).
Slide 15 shows extreme enlargement of paraaortic lymph nodes in a different patient
with disseminated MAC.
Slide 16 shows extensive infiltration of the lamina propria of the small bowel with
distended, so-called “foamy” histiocytes. Slide 17 is an AFB stain of the histiocytes
which are shown to be chock full of MAC organisms.
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