Hematology Flashcards
Bartonella bacilliformis
vectored by sand flies
responsible for Carrion disease consisting of severe anemia (Oroya fecer) followed by verruga peruana (angioproliferative lesions)
disease is located in the Andes mountain region of Peru, Ecuador, and Colombia
The infection increases fragility of infected erythrocytes, leading to anemia
Treat with oral chloramphenicol, doxycycline, or rifampin
Bartonella quintana
agent of trench fever, or five day fever due to the fact it recurs every five days
Causes a severe headache, fever, eakness, and pain in long bones
Spread by the human body louse with no known reservoirs
Associated with immunocompromised patients (bacillary angiomatosis is common)
Treat with oral erythromycin or doxycycline
Bartonella henselae
vectored by fleas
Causes bacillary angiomatosis invovling skin, lymph nodes, liver and spleen.
Reservoirs are cats
Causes “cat scratch disease” which is characterized by chronic regional adenopathy or the lymp nodes
Treatment is “controversial” but treat with azithromycin
Rickettsiaceae general features
Strict intracellular parasites found in cytoplasm
Small, structurally similar to Gram negative although they stain poorly with Gram stain (seen best with Giemsa of Gimenez stains)
Maintained in animal and arthropod reservoirs and are transmitted by ticks, mites, lice and fleas.
Divided into a spotted fever group and a typhus group. Both escape from phagosome using a lipase. The spotted fever groups are continually released through cytoplasmic projections, while the typhus group accumulates intracellularly until cell lysis.
Rickettsia rickettsii
Agent of Rocky Mountain spotted fever
Vectored by dog tick and wood tick (Dermacentor sp)
No evidence of toxin production or overzealous host response, the primary clinical manifestations result from replication in endothelial cells leading to damage and leakage. This leads to hypovolemia leading to reduced organ perfusion.
Cleared by TH1 driven response
Presence is confirmed via antibody detection
Treat with doxycycline or chloramphenicol
Rocky Mountain Spotted Fever
Caused by Rickettsia rickettsii
Peaks in April to September (period of greatest tick activity)
Symptoms develop 7 days following the tick bite. Onset of a high fever and headache that are assoc. with malaise, myalgias, nausea, vomiting, abdominal pain, and diarrhea.
Macular rash develops in 90% of patients. Palms and soles can be involved. Complications inculde neurologic manifestations, pulmonary and renal failure, and cardiac abnormalities.
Treat with doxycycline, chloramphenicol if pregnant
Rickettisialpox
Caused by Rickettsia akari
Transmitted by mites, maintained by rodents in cities, and has a “cosmopolitan distribution”
First, a papule develops at site of mite bite. The papule progresses to ulceration and eschar formation. After a 7-24 day incubation, fever, severe headache, chills, sweats, myalgias, and photophobia occurs.
A generalized papulvesicular rash forms within 2 to 3 days. This looks like smallpox
Resolves without treatment, but doxycycline can be used to expedite healing.
Rickettsia prowazekii
Etiologic agent of epidemic or louse-borne typhus.
Humans are principal reservoir of this disease, and it is spread by the human body louse.
Present in unsanitary conditions (Central and South America, Africa)
Recrudescent disease (Brill-Zinsser disease) can occur years after initial infections
Leads to high fever, severe headache, myalgias, and potential pneumonia, arthralgia, and neurological involvement. A petechial or macular rash develops in 20 to 80% of patients
Diagnosed through serology (MIF test)
Treat with tetracyclines (doxycycline) and controlling lice
Rickettsia typhi
Agent of endemic or murine typhus.
Worldwide distribution, primarily in warm, humid areas.
Rodents are primary reservoir, and the rat flea and cat flea are the primary vectors.
Less severe disease than epidemic typhus, but similar symptoms.
Tetracyclines are used to treat, but most cases resolve even in absence of treatment.
Orientia tsutsugamushi
Agent of scrub typhus, transmitted by mites
Infection also in rodents, which serve as reservoirs
Formerly classified with the Rickettsia
Similar symptoms to other typhus diseases (especially murine/endemic typhus)
Treat with tetracyclines
Human Monocytic Ehrlichiosis
Caused by E. chaffeensis following infection of blood monocytes and mononuclear phagocytes in tissues and organs.
Spread by tick bites
1 to 3 weeks following bite, patients devolop flu-like illness with high fever, headache, malaise, and myalgias. A late onset rash develops in 30 to 40% of patients. Leukopenia, thrombocytopenia, and elevated serum transaminases develop in the majority of patients.
Most patients are hospitalized and need a prolonged recovery time
Ehrlichia
Intraceullar bacteria that parasitize granulocytes, monocytes, erythrocytes, and platelets.
In contrast to Rickettsia and Orientia, Ehrlichia stays in the phagosome by preventing phagolysosome fusion.
Form elementary bodies or reticulate bodies. Elementary bodies form morulae (detected with Giemsa or Wright stains)
Treat with doxycycline
Coxiella burnetii/ Q fever
C. burnetii is extremely stable in harsh environmental conditions and can survive in soil and milk for months to years.
Often associated with dried animal placentas that are aerosolized or contaminated unpasteurized milk.
More likely to occur in ranchers, veterinarians, and food handlers.
Most human infections are aymptomatic or mild, leading to flu-like symptoms.
Chronic Q fever is more serious, and occurs in patients with predisposing conditons such as underlying valvular heart disease or immunosuppression.
Treat with doxycycline
Babesia Species
Agents of babesiosis, a zoonosis infecting deer, cattle, and rodents. Humans are accidental hosts
Located in ticks along the northeastern seaboard of the US.
Infect erythocytes, form tetrads, then lyse the erythrocyte.
Patients experience a general malaise, fever, headache, chills, sweating, fatigue, and weakness. Hemolytic anemia develops, and renal failure may ensue.
Treat with clindamycin combined with quinine
Plasmodium sp.
Four species: P. vivax, P. ovale, P. malariae, and P. falciparum
Infection is initiated by bite of Anopheles mosquito, which introduces sporozoites into the circulatory system.
The parasite replicates in the liver (the exoerythrocytic cycle) and some species can establish a dormant hepatic phase.
When the hepatocytes rupture, they release merozoites which enter erythrocytes.
In the RBC, they progress from a ring, then to a trophozoite, then to a schizont, that culminates in rupture of the RBC.
They also release gametocytes into circulation to be picked up by mosquitoes
P. vivax
Most prevalent of the human plasmodia with widest distribution
Patients experience vague flu-like symptoms with headache, muscle pains, photophobia, anorexia, nausea, and vomiting.
As the infection progresses, the patient gets a typical pattern of chills, fever and malarial rigors called paroxysms
The paroxysms appear every 48 hours (benign tertian malaria)
Invades only young, immature RBCs containing the Duffy blood group antigen.
Infected cells often contain Schuffner dots and golden-brown hemozoin pigment granules
Treat with primaquine to kill hypnozoites in liver
P. ovale
Similar to P. vivax. Infects young, immature, pliable erythrocytes. This distorts the RBCs into ovals.
Found in Africa (mostly) and also in Asia and South America
Also a benign tertian malaria
Diagnose with blood films
Treat with primaquine to kill hypnozoites in liver
P. malariae
Only capable of infecting mature RBCs with rigid cell membranes.
This specieas has “band” and “bar” forms as well as rosettes in the RBC
Less prevalent than other forms of malaria
Has a longer incubation time (up to years) and is a quartan (every 72 hours) or malarial malaria
Does not have a latent liver stage
P. falciparum
No selectivity in RBCs infected and multiple merozoites can infect a single RBC, leading to multiple ring forms
The ring forms are “stuck” on the periphery of the RBC (specific for this organism)
Growing stages are rarely observed as they “stick” to the spleen and liver and micrvasculature
Produces daily (quotidian) chills and fever, then produces malignant tertian malaria (every 48 hours)
Most likely species to kill and most often to cause cerebral malaria
Kidney disease can result called “blackwater fever” leading to kidney failure
Crescentic gametocytes are diagnostic
Filoviruses
Marburg and Ebola viruses
Filamentous, enveloped, negative-strand RNA viruses
Cause severe or fatal hemorrhagic fevers and are endemic in Africa
Widespread hemorrhage leads to hypovolemic shock
Level 4 isolation virus
Flavivirus
Arboviruses (except hepatitis C) spread by mosquitoes
Primarily target monocyte/ macrophage
Enhanced by non-neutralizing antiviral antibody
Humans are dead-end hosts
Viruses haven enveloped, single-stranded, positive-sense RNA.
Replicate in the cytoplasm and bud at internal membranes (opposite of Togaviruses)
Has a “protein coat” of protein E
Synthesizes all proteins as a single polyprotein which is cleaved to active pieces.
Initial viremeia produces flu-like symptoms caused by interferon release
Flavivirus Clinical Syndromes
(Dengue and Yellow Fever)
Most infections are relatively benign, but serious aseptic meningitis and encephalitic or hemorrhagic disease can occur.
Encephalitis viruses include West Nile Virus, St. Loius, Japanese, et c.
Dengue is a hemorrhagic virus that has a worldwide distribution. Dengue Hemorrhagic Fever (DHF) occurs in central and northern South America.
It is also known as break-bone fever. It has high fever, headache, rash, and back and bone pain that last 6 to 7 days. On reinfection with a related strain, it can cause Dengue shock syndrome, which causes a hypovolemic shock
Yellow fever infections are characterized by severe systemic disease, with degeneration of the liver, kidney, heart, as well as hemorrhage. Mortality reaches 50%
There are no treatments other than supportive care
Bunyaviridae
Notable examples include Rift Valley fever, Crimean-Congo, Hantaan, La Crosse, and California encephalitis.
Most are arboviruses with hantaviruses as the notable exception, which is spread by rodents and rodent urine.
They usually cause a nonspecific febrile, flulike, viremia-related illness.
Encephalitis diseases are sudden in onset and lead to fever, headache, lethargy, and vomiting. Seizure disorders are often a sequelae.
Hemorrhagic fevers (RVF) are characterized by petechial hemorrhages, ecchymosis, epistaxis, hematemesis, melena, and bleeding gums. Death occurs in half of patients with hemorrhagic phenomena.
Hantaviruses cause a pulmonary syndrome which is often lethal
Arenaviruses
Include hemorrhagic fever viruses such as the Lassa, Junin, and Machupo viruses.
They infect specific rodent species, and rodents are both the reservoir and the vector
Not arboviruses
They are able to infect macrophages
The hemorrhagic fevers lead to fever, coagulopathy, petechiae, and occasional visceral hemorrhage as well as liver and spleen necrosis, but not vasculitis. They cause no CNS damage
Can treat with ribavirin, but not too helpful
Viruses of White-Cell Neoplasias
Human Herpes Virus-8 is associated with Kaposi Sarcoma, especially in the presence of AIDS patients.
Epstein Barr is associated with a variety of white cell neoplasias including Burkitts, Hodgkins lymphoma
HTLV I leads to Adult T-Cell lymphocytic leukemia, especially in Asian countries and usually around 30 years following infections
