Targeted cells Genus Organism Features Where?

Organism Features Where? Vector Reservoir Transmission Pathogenesis Microscopy Lab tests Clinical manifesta ons Speci c clinical manifesta ons / Treatment Notes
Complica ons
RBCs Plasmodium falciparum Invades RBCs of all Tropical, subtropical Anopheles mosquito Mosquito s ng; Hemozoin pigment in infected RBCs Mul ple ring forms in single Thick and thin peripheral Incuba on 9-30 days. Normocy c anemia. Malignant ter an. Complica ons: Chloroquine, common; most pathogenic Sporo
stages including (F) transfusion; and macrophages; induce host cell to RBCs, stuck to the periphery blood lms. Giemsa/ Splenomegaly, hepatomegaly. Cyclical nature: (1) Cerebral malaria: thrombosis parenteral quinine, (cerebral malaria) zoites
stem cells congenital (cross release TNF; massive destruc on of (Accole forms). Infected Wright staining. (1) Chills, nausea, vomi ng, anorexia, headache; and ischemia caused by s cky RBCs me oquine (inhibit -
placenta); RBCs; type II hypersensi vity mediated RBCs not enlarged. No Fluorescent smears. (2) Febrile stage - several hours, spiking to 40 obstruc ng capillaries, facilita ng nucleic acid synthesis). infec
needle sharing lysis mature trophozoites and Monoclonal an bodies degrees, merozoites released, invading new cytoadherence and coagula on; (2) Artemisinin (form free ve to
schizonts in peripheral to HRP-2 aldolase RBCs; (3) Swea ng stage - fever subsides, Blackwater fever: intravascular radicals and alkylate huma
blood. Sequestered in liver pa ent falls asleep and wakes up feeling be er hemolysis; hemoglobinuria; tubular heme). Atovaquone ns;
and spleen. Crescen c necrosis, renal failure, death (electron transport meroz
gametocytes chain). Proguanil oites -
RBCs Plasmodium vivax Invades RBCs of 80% in S. America and SE Infected RBCs enlarged. Benign ter an. Relapses: liver, (inhibit folate common; most prevalent; infec
one stage (usually Asia Hemozoin pigment in RBCs. kidney and brain damage reductase). hypnozoites can cause ve to
young) One ring per RBC. Mature Primaquine (P. vivax relapse RBCs;
trophozoites, schizonts, liver stages). gamet
gametocytes in peripheral Prophylaxis before ocytes
blood. traveling to endemic -
RBCs Plasmodium ovale Invades RBCs of Africa (also Asia and S. Infected RBCs enlarged and Ter an. Relapses: liver, kidney and regions. Hypnozoites can cause infec
one stage (usually America) oval. brain damage relapse ve to
young) mosq
uitoes
RBCs Plasmodium malariae Invades RBCs of Tropical, subtropical Bar and band-shaped Quartan. Complica ons: (1)
one stage (usually trophozoites. No ring. Nephro c syndrome
young) Merozoites and schizonts
form rose es.
RBCs Babesia micro Pyriform bodies Common in USA Ixodes dammini White- Tick bite. Infected ck bite. Mul ple ring forms (spindle- Blood smears. Incuba on 1-4 weeks. Malaise, fever (no Hemoly c anemia. Renal failure. Mild-moderate: Common in USA.
(oval-shaped with ( ck) footed Transfusion. shaped) in RBCs - early Inocula on of infected periodicity), headache, chills, swea ng, fa gue Splenomegaly, hepatomegaly. atovaquone,
nucleus) - infec ve mouse, Rarely trophozoites. Tetrads blood in hamsters. DNA Higher risk for asplenic pa ents. azithromycin. Severe:
to humans; voles, other transplacental or (Maltese cross forms) in PCR. Serology: an body clindamycin, exchange
merozoites and small perinatal. RBCs - mature trophozoites. detec on transfusion, quinine.
trophozoites - rodents Normocy c hemoly c
infec ve to cks anemia. Low haptoglobin.
High indirect bilirubin. High
re culocytes. High LDH.
High alkaline phosphatase.
High transaminases. Low
platelets.
RBCs Parvovirus B19 Non enveloped. Targets erythroid progenitor cells in B19 IgM and IgG (ELISA). Erythema infec osum: children 3-15 yo; Hosts with sickle cell anemia and Associated with h
Icosahedral capsid. bone marrow (immature, nucleated) Viral DNA (PCR). biphasic illness - ini al ulike disease + immune- hereditary spherocytosis are at disease in children,
Single-stranded and hematopoie c stem cells. Cell Dis nguish rash of B19 mediated phase 2-3 weeks later with rash higher risk of transient aplas c erythema infec osum.
linear DNA. receptor: P an gen (globoside) on from rash of rubella in (slapped cheek rash, later spreading in lacy crisis: decreased RBC count,
erythroblasts, erythroid progenitors, pregnant women: re culate pa ern to arms and trunk) and re culocytopenia. Hydrops fetalis:
endothelial cells, fetal myocardial cells. speci c IgM or viral DNA arthralgia. Infec on in adults: mild febrile malar anemia, edema, hypoxia, conges ve
Cytoly c replica on: suppression of must be detected. rash; polyarthri s; pronounced arthropathy, heart failure, fatal is seronega ve
erythropoiesis, aplas c anemia. Acute especially of wrists, digits, knees, and ankles mother infected before 21 weeks.
infec on of bone marrow, with (more pronounced in women)
abnormal normoblasts, intranuclear
inclusions (accumula on of viral
products).
Macrophages, Leishmania donovani Trypanosome Bangladesh, Brazil, India, Adult female sand y Rodents, Animal-vector- Organism tries to subvert the TH1 Amas gotes (no agellum) Specimens taken from Visceral leishmaniasis (kala-azar) - amas gotes DOC: Sodium (1) Sand y takes a blood
lymphocytes, causing Nepal, Sudan (also involved in anteaters, human. Human- response (suppressing macrophage may be seen inside spleen, lymph nodes, spread to liver, spleen, and bone marrow. s bogluconate. meal (injects
bone marrow leishmaniasis histoplasmosis and sloths, cats, vector-human. ac va on in order to survive inside it) macrophages, esp. In the liver, sternum or iliac Incuba on weeks-years. Malnourished children Amphotericin B. promas gotes into skin).
Macrophages, Leishmania chagasi RMSF) dogs Direct contact and induces the TH2 response, using RES. Obligate intracellular crest bone marrow - or at higher risk. Gradual onset of fever, diarrhea, Cutaneous (2) Promas gotes are
lymphocytes, with infected neutrophils as Trojan horses. forms in macrophages bu y coat of venous anemia, chills, and swea ng. Marked leishmaniasis: phagocytosed by
bone marrow lesion. Lipophosphoglycan (membrane- (Donovan bodies) are not blood. Culture: hepatosplenomagaly. Weight loss, emacia on, miltefosine + macrophages. (3)
Mechanically by associated complex glycolypid) is killed by the macrophage promas gote forms. PCR. edema, ascites. Black sickness: deeply uconazole Promas gotes transform
dog ies. immunosuppressive: inhibits PKC hydroly c enzymes and pigmented granulomatous area of skin. (miltefosine inhibits into amas gotes inside
ac va on and downstream inhibi on resist to the phagolysosome Pancytopenia. Leishmania macrophages. (4)
Macrophages, Leishmania tropica Middle East, focal areas of of MAPK func on, decreasing cytokine acidic milieu. Cutaneous leishmaniasis - amas gotes spread glycolipids) Amas gotes mul ply in
lymphocytes, S. America produc on and release. locally at the site of the bite. Incuba on 2-8 cells (including
bone marrow weeks. Single or mul ple lesions at the site of macrophages) of various
Macrophages, Leishmania major the y bite on face, arms, legs. Starts as red ssues. (5) Sand y takes a
lymphocytes, papule, intensely pruri c, which later ulcerates. blood meal and ingests
bone marrow macrophages infected with
amas gotes. (6) Inges on
of parasi zed cell. (7)
Amas gotes transform into
promas gotes inside
sand y's midgut. (8)
Promas gotes divide in
midgut and migrate to
proboscis.
Macrophages, Leishmania braziliensi Bolivia, Brazil, Peru Mucocutaneous leishmaniasis - amas gotes
lymphocytes, s mul ply locally in the skin and spread to mucous
bone marrow membranes. Starts as cutaneous lesions,
spreading to mucous membranes and related
structures (esp. nasal and oral mucosa).
Secondary bacterial infec ons. Dis gurement.
Lymphocytes, Wuchereria bancro i Nematode - round Tropical, subtropical. Asia, Anopheles (also Mosquito bite Micro lariae (diagnos c Micro lariae in blood: Blockage of lympha c system, causing Chronic: enlargement of lymph An parasi c drugs: (1) Third-stage larva enters
lympha cs worm, mul cellular SE Asia, Caribbean. Plasmodium), Aedes stage) are sheathed and the Giemsa stain. accumula on of lymph and edema in the arms, nodes (extremi es, scrotum, diethylcarbamazine, skin through mosquito
- causing lariasis (also dengue virus), p of their tail is devoid of Eosinophilia. the legs, and the groin. Fever, lymphangi s, testes); abscess; blockage of ivermec n bite. (2) Adult organisms
and Culex nuclei. Adult worms appear lymphadeni s, chills, recurrent febrile a acks. lympha c vessels; secondary spread through the
mosquitoes thread-like in lympha c In ammatory response to moul ng larvae and bacterial infec on, in ammatory lympha c system, where
vessels and ssues. dead adult worms inside lympha c vessels. reac on causing ssue damage and they undergo sexual
Lymphocytes, Brugia malayi Micro lariae (diagnos c hypertrophy. Elephan asis. reproduc on. (3)
lympha cs stage) are sheathed and the Micro lariae - the
p of their tail is lled with daughters - are released in
nuclei. Adult worms appear the blood at night and
thread-like in lympha c spread through the blood
vessels and ssues. circula on. (4)
Micro lariae are ingested
by mosquito in a blood
meal. (5) Micro lariae
grow as rst-stage and
second-stage larvae, and
migrate to the proboscis.

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 Endothelial Ricke sia ricke sii Obligate Common in USA, Hard ck (dog ck or Ticks, wild Tick bite (1) Adhesion to endothelial cells Cell wall similar to Gram Direct uorescent assay Generalized maculopapular pink rash, becoming Pinpoint hemorrhages leading to Doxycycline. Rifampin.
cells intracellular especially during warm wood ck - rodents mediated by outer membrane protein nega ve bacteria, but stains of skin biopsy. petechial (leakage of RBCs - "spo ed fever") or encephali s, pneumoni s, cardiac No vaccine.
parasite causing months. Endemic in North Dermacentor) OmpA. (2) Uptake by zipper-like poorly with Gram (they are Microimmuno uorescen purpuric, appearing on wrists, ankles, palms, arrhythmia, nausea, abdominal
Rocky Mountain Carolina, Oklahoma, process. (3) Ricke sia in endosome. (4) intracellular). Best stained ce test detects and soles, later spreading to the trunk. Edema. pain. Elderly pa ents:
spo ed fever. Arkansas, Tennessee, Escape from endosome via PLD. (5) with Giemsa/Gimenez an bodies against OmpA Non-speci c: high fever, sever headache, splenomegaly, DIC and sep c shock
Energy parasite: Missouri. Bacterial mul plica on by binary and LPS. IgM and IgG myalgia, respiratory symptoms, nausea, (endotoxin release), and death (20%
uses host ATP, CoA, ssion in endothelial cells. (6) Release an bodies (ELISA and vomi ng, diarrhea. if untreated)
NAD, and amino by focal lysis or cell lysis, or by PCR). Weil Felix test for
acids. Divide by penetra on to adjacent cell. (7) heterophile an bodies
binary ssion Thrombosis, leakage of RBCs from (an gens of Proteus
within host cell blood vessels vulgaris - similar to
cytoplasm and Ricke sia but easier to
nucleus grow). Also Giemsa stain
and
immunohistochemistry
of endothelial cells.
Monocytes Ehrlichia cha eensi Intracellular Common in USA: Lone Star ck White-tailed Tick bite Intracytoplasmic inclusions Nucleic acid Late onset rash (unlike Ricke sia). Flulike illness Fulminant sep c syndrome in
s organism. Causes Southeast, Mid-Atlan c, (Amblyomma deer, (Morulae) - less than 10%. ampli ca on. Serology. 1-2 weeks a er bite, with high fever. immunocompromised.
human monocy c Midwest, South-Central americanum) chipmunks, Leukopenia, thrombocytopenia, elevated serum
ehrlichiosis voles, transaminases.
canines
Granulocytes Anaplasma phagocyto Intracellular Common in USA, Ixodes ?? ( ck) Small Tick bite Hijacking of host cell processes: Intracytoplasmic inclusions Giemsa staining of Late onset rash (unlike Ricke sia). Leukopenia. Fulminant sep c syndrome in
phillum organism. Causes especially in warm mammals inhibi on of spontaneous apoptosis of (Morulae) - 25-75%. peripheral blood. Nucleic Thrombocytopenia. Elevated serum immunocompromised. Peripheral
human granulocy c months: Upper Midwest, neutrophils (in order to survive inside acid ampli ca on. transaminases. neuropathies.
anaplasmosis Northeast, Atlan c them); inhibi on of granulocyte phox Serology: IgM/IgG
gene transcrip on; downregula on of detec on
phagocyte oxidase ac vity (ROS);
decrease of neutrophil binding and
transmigra on through endothelium;
inhibi on of phagocytosis and
autophagy. Infec on s mulates
neutrophil recruitment, ac va on,
chemokine secre on, and
degranula on, leading to in amma on
and ssue damage, and then to
secre on of IFN-gamma, which
ac vates macrophages and causes
further damage to ssues.
Coxiella burne i Unlike Ricke siae: Worldwide. Asymptoma c Shed by animals Sheep and Inhala on of Spread through blood. Immuno uorescence No rash. Acute pneumonia (atypical Acute: doxycycline.
not transmi ed infec on of livestock in during parturi on goats (esp. airborne assay and ELISA for pneumonia), u-like symptoms. Chronic Chronic:
through insect common in USA. In placenta par cles. an bodies. PCR. endocardi s (suspect in pa ent with hydroxychloroquine +
vectors; no rash. and fetal Consump on of endocardi s symptoms but nega ve blood doxycycline
Biphasic during membrane) unpasteurized culture). Granulomatous hepa s associated
infec on: Phase I - milk and animal with endocardi s (complica on of Q fever).
intact LPS (more products
virulent, severe
infec on); Phase II -
no O an gen in LPS.
Seen in shepherds,
farmers, and vets
Monocytes Arbovirus avivirida Worldwide - S. America, C. Aedes aegyp (also Mosquito bite(1) Dengue type 1 infects monocytes Incuba on 4-8 days. Severe bone and joint pain Dengue hemorrhagic fever or No an viral. Pa ent infected with one
e (dengue) America, Puerto Rico, liriasis) (2) Recovery, with an body to type 1 ("break bone disease"). Maculopapular or Dengue shock syndrome, on Suppor ve care only. subtype will recover with
Texas, Florida, SE Asia, Later: (3) Challenge with dengue type erythematous rash. Non-speci c: high fever, reinfec on with another type of No vaccine yet. an bodies (IgG - long-
Paci c, India 2, which also infects monocytes headache, malaise, arthralgia (immune complex dengue: severe illness, shock, term) to that subtype only.
directly on its own (4) Dengue type 2 + deposi on), nausea, vomi ng. Symptoms last hemorrhage, death (10%). Children
an body to type 1 form a complex (5) for 6-7 days. Recovery may be followed by and elderly are more at risk.
Virus-an body complex enters prolonged fa gue or depression.
monocytes via Fc receptor (6)
Increased produc on of cytokines +
increased infec on with type 2 (7)
Dengue hemorrhagic fever / Dengue
shock syndrome
Lymphocytes Herpesvirida Epstein- Gamma Human-human, (1) Infec on of epithelial cells or Atypical lymphocytes Atypical lymphocytes Moderate hepatosplenomegaly. Fa gue for Spleen rupture, even with minor EBV encoded proteins for
e Barr herpesvirus (like via saliva oropharynx. (2) Spread to underlying (Downey cells) demonstrate (Downey cells) in months. Hepa c dysfunc on with jaundice and trauma. Burki 's lymphoma: poorly latency: (1) EBNA-1
HHV-8 - Kaposi (kissing) lymphoid ssue (tonsils, adenoids). (3) T cell ac va on. peripheral blood. elevated liver enzymes. Depends on state of di eren ated monoclonal B cell (Epstein-Barr nuclear
sarcoma virus). Bind to CD21/CR2 receptor Monospot test for cellular immunity, in the face of an overac ve B lymphoma of the jaw and face, an gen 1), incorpora ng
Enveloped double- (complement receptor) of mature B heterophile an bodies cell response: (1) Vigorous cellular immunity will endemic in children living in EBV genome to host
stranded DNA virus. cells. (4a - minority) Ly c infec ons, (posi ve in EBV; result in a "civil war" between infected B cells malarial regions of Africa. Hairy oral chromosome, which allows
Latent and with viral replica on in B cells, nega ve in CMV). ELISA. and protec ve T cells = infec ous leukoplakia: raised corrugated viral DNA to be passed on
recurrent followed by lysis of target cells and Speci c an bodies to mononucleosis (fever, fa gue, sore throat, tonsil white lesions of the tongue and to daughter cells. (2) LMP1
infec ons. release of virus, using host membrane viral capsid an gens, and lymph node enlargement, photophobia). (2) mouth, opportunis c infec on in (latent membrane protein),
to form envelope. (4b - majority) early an gens, EBNA: Normal cellular immunity = asymptoma c. (3) AIDS. EBV-induced driving B cell ac va on and
Latent infec ons, with memory B cells, IgM to VCA - acute Poor cellular immunity = Burki 's lymphoma, lymphoprolifera ve disease: in prolifera on by mimicking
where virus persists as an extra- primary infec on; IgG to nasopharyngeal cancer. (4) No cellular immunity immunocompromised pa ents, in CD40, and preven ng
chromosomal episome. (5) B cell VCA and no EBNA - = oral hairy leukoplakia pa ents with congenital T cell apoptosis by ac va ng
prolifera on will result in an chronic primary dysfunc on, transplant pa ents. Bcl-2. (3) EBNA-2 (Epstein-
uncontrolled popula on of polyclonal infec on; IgG to VCA and Nasopharyngeal carcinoma: EBV Barr nuclear an gen 2),
B cells (heterophile an body). (6) T to EBNA - past infec on DNA found in tumor cells of promo ng B cell ac va on
cells are ac vated in response to the and lifelong immunity. epithelial origin, endemic in Asia and replica on, and
infec on. (7) Virus persists in B cells among adults. turning on transcrip on of
forever, and may be reac vated when host cell genes that encode
memory B cells are ac vated in tonsils cyclin D. (4) Viral
and pharynx, and may be shed in saliva homologue of IL-10, which
inhibits macrophages,
dendri c cells, and
an viral TH1 cells

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 Monocytes, Herpesvirida Cytomegal Beta herpesvirus Human-human, Evasion and suppression of immune Infected cell: gigan sm of Demonstra on of viral CMV mononucleosis: asymptoma c in healthy Immunosuppressed pa ents: coli s, Ganciclovir (or
bone marrow e ovirus (like HHV-6) via all body response. Infects dendri c cells and cell and nucleus. Nucleus: an gen or virus in blood, people; fever, lymphadenopathy, hepatomegaly. esophagi s, choriore ni s, valganciclovir):
progenitors, uids: impair an gen processing and large basophilic inclusions urine, ssues, bronchial pneumoni s, hepa s, primary guanosine nucleoside
broblasts, transplacental, presenta on (downregula on of MHC with halo (owl's eye). washings. Fluorescent infec ons or reac va on of latent analogue targe ng
epithelial cells neonatal, saliva I and MHC II). Produces homologues of Cytoplasm: ill-de ned an body stain on infec ons. Congen al cytomegalic DNA polymerase
(schoolchildren), TNF receptor, IL-10, and MHC I. basophilic inclusions. Found infected cells. inclusion disease, acquired from (compe ve inhibi on
genital (primary Produces ligand that binds KAR and in lung and kidney Demonstra on of owl's mother without protec ve of DNA synthesis),
a er 15 yo), blocks KIR on NK cells (cannot get epithelium and eye inclusions in an bodies: jaundice, ac vated by viral
iatrogenic killed by NK cells). Virus persists in endothelium, alveolar cytomegalic cells. hepatosplenomegaly, rash, anemia, protein kinase.
(transfusion, leukocytes. macrophages, neurons Monospot test for thrombocytopenia, microcephaly, Foscarnet: inhibits
transplant) heterophile an bodies periventricular calci ca on. DNA polymerase, RNA
(nega ve in CMV; polymerase, and
posi ve in EBV). DNA reverse transcriptase,
PCR. IgM in neonatal doesn't require
infec ons. CMV-speci c phosphoryla on for
an bodies: (1) IgM- and ac va on. Cidofovir:
IgG- = no infec on. (2) cytosine nucleo de
IgM+ and IgG- = recent analogue, doesn't
ac ve primary infec on require
(or reac va on of latent phosphoryla on for
infec on if Ab ac va on.
produc on has waned).
(3) IgM- and IgG+ = past
exposure. (4) IgM+ and
IgG+ = ongoing primary
infec on where IgM is
s ll ac vely produced (or
reac vated latent
infec on)
Bartonella henselae Gram nega ve Cat scratch or Spread via lympha cs to draining Don't stain well with Immunocompetent pa ents - cat scratch Immunocompromised pa ents - DOC: Erythromycin or
and rods. Cat scratch bite. Cat ea regional lymph nodes, where bacteria Gram. Warthin Starry disease. Small papule at site of inocula on, 3-10
bacillary angiomatosis, sca ered azithromycin. Also,
quintana disease. feces. proliferate. In immunocompromised silver stain. days a er. Chronic regional adenopathy, cutaneous papules and nodules, doxycycline.
pa ents, host response cannot control Immuno uorescence. granulomatous and suppura ve host response. violaceous, resembling pyogenic
infec on, and bacteria mul ply and Serology. PCR Self-resolving. granuloma, with sepsis or localized
disseminate. ampli ca on. infec on of the skin, liver, viscera.
Also subacute endocardi s (post-
infec on complica on) and hepa c
peliosis.
Endothelial Bunyavirida Hantavirus Enveloped virus, Rodents Through rodent (1) Entry through respiratory or Virus neutraliza on (1) Prodrome: fever, myalgia, headache, chills, Hantaan virus: hemorrhagic fever Ribavarin in early
cells e es with segmented, (deer excreta: diges ve tract. (2) Virus mul plica on assay. IgM in acute ver go, nausea, vomi ng. (2) Cardiopulmonary with renal syndrome. Sin Nombre infec on
nega ve sense, mouse) inhala on of in lung endothelium, follicular infec on. Fourfold phase: cough, fever, dyspnea, tachypnea, virus: hantavirus pulmonary
single-stranded aerosols. dendri c cells of the spleen and lymph increase in IgG. Tetrad of tachycardia, rales; CXR - non cardiac pulmonary syndrome.
RNA. nodes. (3) An bodies damage hematologic ndings in edema, pleural e usion, cardiac silhoue e not
endothelial cells and increase vascular hantavirus pulmonary enlarged; inters al edema, peribronchial
permeability. (4) Leakage of protein- syndrome: cu ng
rich plasma into lungs and pleura thrombocytopenia,
leukocytosis with
neutrophilia and le
shi ,
hemoconcentra on,
circula ng immunoblasts
and plasma cells
Macrophages Histoplasma capsulatu Dimorphic fungus Endemic in Ohio and Inhala on of (1) Yeast survives phagolysosomal Direct microscopic Culture to demonstrate Low intensity exposure: 90% asymptoma c, self- Immunocompromised pa ents Suppor ve care. For Infec on associated with
m (mold/mycelial Mississippi fungi from soil killing by alkalinizing lysosomes and examina on of bronchial dimorphism. An bodies limi ng primary infec on of the lung. Acute (AIDS, transplant, steroids): febrile complicated infec ons disturbance of bird roost,
form with enriched with inac va ng degrada ve enzymes of washings, sputum, bone by immunodi usion, form: fever, chills, headache, myalgia, cough for illness, hepatosplenomegaly, only: itraconazole, disturbance of bat caves
tuberculate conidia bird and bat phagolysosomes: allows yeast to marrow, lymph node biopsy, complement xa on. a few weeks. Heavy exposure: chronic dissemina on to skin, CNS, amphotericin B (spelunking), demoli on of
- outside body; droppings. No mul ply. (2) Yeasts disseminate to using Giemsa/Wright stain. An gen detec on in progressive form - fever, cough for weeks, adrenals, painless ulcers on mucous buildings
yeast - inside human-human. liver, spleen, lymph nodes, bone urine (ELISA). Nucleic malaise, hemoptysis, weight loss (resembles membranes, arthri s, arthralgias,
macrophages, marrow via lympha cs (primary lesion acid hybridiza on, PCR. tuberculosis), CXR - pulmonary in ltrates with rarely medias nal brosis
causing a chronic is like tuberculosis - calci ed node). (3) hilar or medias nal lymphadenopathy
granulomatous Yeasts remain viable in old lesions and
reac on) can be reac vated later in
immunocompromised pa ents.
Immune response: APC secretes IL-12,
ac vates TH1-mediated immunity -
TH1 prolifera on via IL-2, macrophage
ac va on via secre on of IFN-gamma,
leading to intracellular killing of yeast
and to secre on of TNF to s mulate
other macrophages - Type IV
hypersensi vity reac on to
histoplasmin an gen.

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