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BHL Week 4 Questions

Terms in this set (61)

CMV (The clinical features described are typical of congenital cytomegalic inclusion disease caused by cytomegalovirus (CMV). Among the beta-herpes viruses, CMV is the one associated with congenital infection. CMV when grown on human fibroblastic cells produces a characteristic cytopathic effect. Many affected cells become enlarged. Giant cells with large intranuclear acidophilic inclusions (owl eye inclusions) and perinuclear cytoplasmic inclusions are seen. Virus replicates very slowly and infection spreads from cell to cell. It may take several days for the entire monolayer to be infected. Inclusion-bearing cytomegalic cells can be demonstrated in centrifuged deposit of urine and in other clinical samples from infected tissues.

In the US, up to 80% of adults show antibodies to the virus indicating high prevalence of the infection. CMV is the most frequent congenitally transmitted virus in the country. Each year about 40,000 children are born with congenital cytomegalovirus infection. Congenital CMV disease causes estimated 400 deaths each year and leaves approximately 8,000 with permanent disabilities like mental retardation, hearing loss, and ocular impairment. Fetal death or generalized cytomegalic inclusion disease results when the mother acquires and transmits primary CMV infection to the fetus during the first trimester of pregnancy. Reactivated maternal infections may not cause fetal damage. Perinatal infection of the new born can occur from the mother's birth canal or breast milk.

Spread of the virus is predominantly by close contact and through oral and respiratoy routes. In immunocompetent persons usually the infection is subclinical. The virus sometimes causes heterophile antibody negative mononucleosis. This most commonly follows transfusion of CMV infected blood (post-transfusion mononucleosis). CMV is an important pathogen in patients with AIDS. The already weakened immune response is further damaged by the nonspecific CMI-inhibiting effect of CMV. Disseminated and often fatal infections are produced with manifestations such as chorioretinitis, gastroenteritis and pneumonia. Immunosuppressed individuals like organ transplant recipients are also at high risk of developing severe CMV disease. Often development of illness may be due to reactivation of their own latent virus.)
CCR5
(CCR5 is a chemokine receptor that binds to several chemokines including MIP-1alpha, MIP-1beta and RANTES. CCR5 is necessary for HIV entry into the host cell. CCR5 is expressed by macrophages, dendritic cells, and CD4 T cells. It is thought to be the major co-receptor for establishing primary infection, since individuals who are homozygous for a mutation in CCR5 appear to be resistant to infection by HIV. For example, the CCR5-Delta32 deletion mutation seems to confer resistance against HIV-1 by blocking its attachment to CCR5 so that HIV cannot gain entry to the cell. Development of drugs directed at chemokine receptors is thus an active area of research.

CXCR4 is the other major co-receptor for HIV. Lymphotropic HIV uses CXCR4 found on T cells and requires a high density of CD4 on the cell surface. CXCR4 also binds the CXC-chemokine stromal-derived factor-1 (SDF-1) as a co-receptor. Both co-receptors are G-coupled proteins with 7 transmembrane spanning domains.

Mac-1, also called CD11b/CD18, is stored in specific granules that are shuttled to the granulocyte surface. It exists as a chemoattractant activation-dependent molecule that undergoes a conformational change upon stimulation. Until stimulation occurs, it remains in a resting, non-adhesive state. Mac-1 is a β2 integrin.

SDF-1 is a small chemokine of the CXC subfamily that is produced constitutively by bone marrow stromal cells and has an important role in early stages of B cell development. It is a growth factor for B cell progenitors and a chemotactic factor for T cells, monocytes, CD34+ hematopoietic progenitor cells, mature megakaryocytes, and dendritic cells.

Interleukin-8 or IL-8, a CXC chemokine, is an 11-kDa homodimer of 99 amino acids that is also known as monocyte-derived neutrophil chemotactic factor (MDNCF). It is an important mediator of neutrophil, lymphocyte, and basophil chemotaxis and activation. It is released from several cell types in response to an inflammatory response.)
Hypermutability (The hypermutability of HIV, which mutates at a rate 1,000,000 times as great as that of eukaryotic DNA genomes, is important to the pathogenesis of HIV. The high error rate of HIV reverse transcriptase in vitro translates to approximately 5 to 10 errors per HIV genome per round of replication in vivo. This high error rate suggests that misincorporation by HIV reverse transcriptase is, at least in part, responsible for the hypermutability of the AIDS virus. Researchers hope that our understanding of the process may provide a basis for the systematic construction of antiviral nucleosides.

In gene conversion, DNA segments are copied so that one sequence replaces sequences in another gene on the same chromosome. Studies of the sequences of different alleles have shown that the same sequences are found within several genes on the same chromosome, providing evidence for gene conversion.

Gene duplication is the creation of an extra copy of a gene. This is a key mechanism in evolution. Once a gene is duplicated, the identical genes can undergo changes and diverge to create 2 different genes. Duplications typically arise from an event termed unequal crossing-over that occurs between misaligned homologous chromosomes during meiosis.

Antigenic shift is the appearance of a new assortment of genes. This type of reassortment happens rarely and can be devastating, since shift produces a virus strain with a combination of surface antigen proteins to which the human population will have little or no immunity.

Antigenic drift is caused by point mutations in the genes of microbes, such as the influenza virus. Every 2 to 3 years, a variant arises with mutations that allow the virus to evade neutralization by antibodies in the population. As new variants appear, they replace the previous variant so that within about 4 years, a given individual can be re-infected with an antigenic variant that has been gradually generated by infection of other individuals. This results in local epidemics.)
Breakbone fever (Dengue fever virus and Powassan virus are members of the family Flaviviridae. Flaviviruses are enveloped viruses with icosahedral symmetry. The genome consists of a linear single stranded RNA molecule and replication occurs in the cytoplasm. Dengue fever virus is transmitted by the mosquito and is associated with bone break fever and dengue shock syndrome. Bone break fever is characterized by headache, myalgia, arthralgia, and rash. Secondary exposure can result in dengue shock syndrome and is characterized by gastrointestinal hemorrhage.

Powassan virus is associated with tick-borne virus encephalitis. Ixodes tick is the vector for Powassan virus. Domestic animals can play a role in the spread of the disease, as the tick can bite the domestic and farm animals and humans can be infected by the ingestion of raw milk or tick bite.


Coxsackievirus type A and coxsackievirus type B are members of the Picornaviridae family. Picornaviruses are naked viruses with an icosahedral nucleocapsid. The genome consists of single molecule of single stranded RNA. Coxsackievirus type A is associated with herpangina, which is commonly seen in children. Herpangina is a severe febrile pharyngitis characterized by vesicles or nodules primarily on the soft palate.

Coxsackievirus type B is associated with Bornholm disease seen mainly in older children and young adults. Bornholm disease is myositis and is also called Pleurodynia. It is characterized by paroxysms of stabbing pain in the chest muscles and abdomen muscles.

Variola virus is a brick-shaped virus with a single linear molecule of double stranded DNA and is a member of the Poxviridae family. Variola virus was the causative agent of smallpox that multiplied in the lymph nodes. Smallpox is an ancient disease that is eradicated.)
Plasmodium falciparum. (The banana-shaped gametocyte (red arrow) is pathognomonic for P. falciparum.
Malaria is an acute and sometimes chronic infection of the blood stream caused by the parasite of the genus Plasmodium. The 4 species of plasmodium causing human malaria include: Plasmodium falciparum, P. vivax, P. ovale, and P. malariae. The common presenting symptoms of malaria include chills and fever, which are often associated with splenomegaly. In the early stages of the disease, the febrile episodes occur irregularly but eventually become more synchronous, assuming the usual tertian (P. vivax, P. Falciparum, P. ovale) and quartan (P. malariae) periodicity. Patients with malaria may develop anemia and other manifestations, including diarrhea, abdominal pain, headache, and muscle aches and pains.

P. falciparum malaria can result in high parasitemias, which can lead to severe hemolysis with hemoglobinuria and profound anemia. Erythrocytes infected with growing trophozoites, schizonts of P. falciparum, become sequestrated in small vessels of the body, and they may lead to occlusion of these vessels, causing symptoms related to capillary obstruction and tissue anoxia. Involvement of the brain is known as cerebral malaria, in which the patient becomes disoriented, progressing to delirium, coma, and often death.

Malarial parasites undergo sexual phase (sporogony) in anopheles mosquitoes and an asexual stage (schizogony) in humans that results in the production of schizonts and merozoites. In the blood stream, some merozoites eventually differentiate into gametocytes (gametogony), which when ingested by female anopheline mosquitoes, mature into male microgametes and female macrogametes. Fusion of a microgamete and a macrogamete results in the formation of the motile ookinete, which migrates to the outside of the stomach wall and forms an oocyst. Within the oocyst, numerous spindle-shaped sporozoites are formed. The mature oocyst ruptures into the body cavity, releasing the sporozoites, which then migrate through the tissues to the salivary glands, from which they are injected into the vertebral host as the mosquito feeds. The time required for the development in the mosquito ranges from 8 to 21 days.

The sporozoites injected into the vertebrate host reaches the hepatic parenchymal cells within minutes and initiate the proliferative phase known as exoerythrocytic schizogony. Release of merozoites from ruptured hepatic schizonts initiates the blood stream infection or erythrocytic schizogony and eventually the clinical symptoms of malaria. P. vivax and P. ovale differs from P. falciparum and P. malariae in that true disease relapses of the former species may occur weeks to months following subsidence of previous attacks. This occurs because of renewed exoerythrocytic and eventually erythrocytic schizogony from latent hepatic sporozoites, which are known as hypnozoites. Recrudescences of disease due to P. falciparum or P. malariae called recrudescences arise from an increase in the number of persisting blood stage forms to clinically detectable levels, not from persisting liver stage forms. P. vivax and P. ovale parasites primarily infect young erythrocytes, whereas P. malariae affects older erythrocytes, and P. falciparum infects erythrocytes of all stages.)
Integrase and reverse transcriptase, which are carried in the virion. (The retroviral life cycle begins when the virion lands on specific receptors and enters the cell, where the virion coat is removed in the cytosol. The virus particle contains two copies of an RNA molecule. One of the copies is designated the (+) strand. In addition to the (+) strand, the virion also carries into the host cell the enzyme reverse transcriptase and a non-covalently attached tRNA molecule. The enzyme reverse transcriptase has three major activities: RNA-directed DNA synthesis, DNA-directed DNA synthesis, and RNA hydrolysis. The RNA molecule that the virion brings into the cell must be duplicated for the viral life cycle to continue. The steps of this process are as follows:

Using the tRNA that the virion brings into the cell, the transcriptase engages in DNA synthesis in the 5' to 3' direction. This gives a short segment of DNA that is attached to the tRNA. This DNA is termed (-) DNA. RNAase activity of the transcriptase removes RNA bases paired with the newly formed DNA. The (+) RNA strand contains repeated sequences at each of its termini. The newly formed DNA-tRNA hybrid molecule pairs with the other end of the (+) RNA strand and the RNA is reversed transcribed into DNA. Most of the (+) RNA strand that is now paired with the newly synthesized DNA is hydrolyzed by the RNAase activity of the transcriptase. The remaining small segment of RNA is used as a primer to replicate a (+) DNA strand from the (-) DNA strand used as template. Any residual RNA is hydrolyzed. The newly formed (+) DNA strand pairs with the opposite end of the (-) DNA strand and primes the synthesis of the remaining (+) DNA strand. Each end of the (-) DNA strand consists of long terminal repeat sequences termed long terminal repeats (LTR).

For it to function, the formed linear DNA must travel to the nucleus and be integrated into the host genome. The integration reaction is catalyzed by the viral product integrase, which is carried in the virion along with the reverse transcriptase. The integration of the viral DNA occurs at random sites in the host genome. Integrated proviral DNA is transcribed by the host enzymes to make viral RNAs. These RNA molecules can function both as mRNA and as inserts to make more virion particles.)
Histoplasma capsulatum (The patient's condition is most likely to be acute pulmonary histoplasmosis acquired by exposure to bat guano containing spores of Histoplasma capsulatum. In the U.S., infections by H.capsulatum are highly endemic in Ohio and Mississippi valleys and also in localized foci in mideastern states. Infection occurs due to inhalation of aerosols containing the fungal conidia (spores). Person to person transmission does not occur. Excreta of birds and bats are known to accelerate the growth of the mycelial forms and sporulation of the fungus. Bat guano can be a good source of the spores, as the fungus can colonize in the gastrointestinal tract of bats. Exposure may result in asymptomatic infection or symptomatic disease. The extent of disease depends on the number of conidia inhaled and the host's cellular immunity. Pulmonary infection is the primary manifestation of infection. It is often self-limited, with flu-like symptoms from which recovery occurs without any specific treatment. Inhalation of a large number of spores may result in severe pulmonary disease with acute respiratory distress syndrome. Thermally dimorphic fungi are fungi that occur in 2 morphological forms at different temperatures. Yeast forms are seen in tissues and when grown on enriched media at 37°C. Mycelial forms are seen in the soil and when grown on Sabouraud's or similar media at 25 to 30 degrees. Description of the tissue form given in the question is typical of H.capsulatum. Histoplasmosis is worldwide in distribution. It is more prevalent in North and Central America. Occupation and travel-associated outbreaks of acute histoplasmosis have been reported in U.S. Other than acute pulmonary infection, main clinical manifestations of the disease are chronic cavitary pulmonary histoplasmosis and disseminated histoplasmosis. Chronic cavitary pulmonary histoplasmosis simulates pulmonary tuberculosis and develops in people with pre-existing pulmonary conditions like emphysema or chronic obstructive pulmonary disease (COPD). Disseminated histoplasmosis occurs in people with impaired cell-mediated immunity, as in HIV positive individuals, immunosuppressed individuals, and the elderly. Dissemination affects the reticuloendothelial system and may involve other organs including skin and mucous membranes.

Aspergillus fumigatus is a mold and Cryptococcus neoformans is yeast. Neither are dimorphic fungi. Coccidioides immitis is one of the thermally dimorphic fungi and causes coccidioidomycosis, endemic in the dry arid regions of Southwest U.S. The tissue form of the fungus does not resemble that of H.capsulatum and occurs as large spherules (10-80 microns) with a thick doubly refractile wall containing endospores. Blastomyces dermatitidis is similar to H. capsulatum in many respects. However, it appears in tissue as a broad-based yeast.)
Cerebral toxoplasmosis (The patient in this case is immunocompromised due to the immunosuppressive therapy and is prone for opportunistic infections. Cerebral toxoplasmosis is caused by the protozoa Toxoplasma gondii. In immunocompetent patients, most infections are asymptomatic or self-limiting. Congential toxoplasmosis occurs following primary maternal infection early in the pregnancy causing cerebritis in the fetus with production of multi-focal cerebral necrotizing lesion that may calcify producing severe damage to the brain. Infection with T. gondii is one of the most common causes of neurological symptoms and morbidity in patients with AIDS. CT and MRI show multiple ring enhancing lesions. The brain shows multiple abscesses often involving the cerebral cortex. Acute lesions consist of central foci of necrosis with variable petechiae surrounded by acute and chronic inflammation, macrophage infiltration, and vascular proliferation. Both the tachyzoites and encysted bradyzoites may be found at the periphery of necrotic foci. The organisms are usually seen by routine H& E and Giemsa stains, but can be readily recognized by immunocytochemical methods.

Cytomegalovirus causes typically sub-acute encephalitis in immunosuppressed patients. Although any type of cell in the CNS can be infected by CMV, there is a tendency for the virus to localize in the ependymal and sub-ependymal regions of the brain causing severe hemorrhagic necrotizing ventriculi-encephalitis and choroids plexitis. Prominent cytomegalic cells with intranuclear and intracytoplasmic inclusions can be readily identified by conventional light microscopy, immunocytochemistry, or in-situ hybridization.

Cryptococcal meningitis is caused by the fungus Cryptococcus neoformans. It occurs in increasing frequency in association with AIDS and may be fulminant and fatal in as little as 2 weeks or indolent, evolving over months or years. The mucoid encapsulated yeasts can be visualized in the C.S.F by India ink preparation. The brain shows chronic meningitis affecting the basal leptomeninges, which are opaque and thickened. Sections of the brain disclose a gelatinous material within the sub-arachnoid space and small cysts within the parenchyma. Parenchymal lesions consist of aggregates of organism within the expanded peri-vascular spaces associated with minimal or absent of inflammation or gliosis. The meningeal infiltrates consists of chronic inflammatory cells, fibroblasts admixed with cryptococci, which can be seen well with PAS, mucicarmine or silver stain.

Fungal disease of the C.N.S is encountered primarily in immunocompromised patients. Aspergillosis and mucormycosis has marked predilection for invasion of blood vessel walls causing thrombosis producing hemorrhagic infarction with subsequent ingrowth of the fungus. Cerebrospinal fluid examination will not be of any diagnostic value. Numerous septate hyphae invading blood vessels with acute inflammatory reaction can be seen in tissue sections.

HSV encephalitis can cause necrosis of the left temporal lobe but does not exhibit ring-enhancing lesions.)
Cryptococcal meningitis (The patient in this case is immunocompromised due to the immunosuppressive therapy and is prone for opportunistic infections. Cryptococcal meningitis is caused by the fungus Cryptococcus neoformans. It occurs in increasing frequency in association with AIDS and may be fulminant and fatal in as little as 2 weeks or indolent, evolving over months or years. The mucoid encapsulated yeasts can be visualized in the C.S.F by India ink preparation. The brain shows chronic meningitis affecting the basal leptomeninges, which are opaque and thickened. Sections of the brain disclose a gelatinous material within the sub-arachnoid space and small cysts within the parenchyma. Parenchymal lesions consist of aggregates of organism within the expanded peri-vascular spaces associated with minimal or absent of inflammation or gliosis. The meningeal infiltrates consists of chronic inflammatory cells, fibroblasts admixed with cryptococci, which can be seen well with PAS, mucicarmine or silver stain.

Cytomegalovirus causes typically sub-acute encephalitis in immunosuppressed patients. Although any type of cell in the CNS can be infected by CMV, there is a tendency for the virus to localize in the ependymal and sub-ependymal regions of the brain causing severe hemorrhagic necrotizing ventriculi-encephalitis and choroids plexitis. Prominent cytomegalic cells with intranuclear and intracytoplasmic inclusions can be readily identified by conventional light microscopy, immunocytochemistry, or in-situ hybridization.

Fungal disease of the C.N.S is encountered primarily in immunocompromised patients. Aspergillosis and mucormycosis has marked predilection for invasion of blood vessel walls causing thrombosis producing hemorrhagic infarction with subsequent ingrowth of the fungus. Cerebrospinal fluid examination will not be of any diagnostic value. Numerous septate hyphae invading blood vessels with acute inflammatory reaction can be seen in tissue sections.

Cerebral toxoplasmosis is caused by the protozoa Toxoplasma gondii. In immunocompetent patients, most infections are asymptomatic or self-limiting. Congential toxoplasmosis occurs following primary maternal infection early in the pregnancy causing cerebritis in the fetus with production of multi-focal cerebral necrotizing lesion that may calcify producing severe damage to the brain. Infection with T. gondii is one of the most common causes of neurological symptoms and morbidity in patients with AIDS. CT and MRI show multiple ring enhancing lesions. The brain shows multiple abscesses often involving the cerebral cortex. Acute lesions consist of central foci of necrosis with variable petechiae surrounded by acute and chronic inflammation, macrophage infiltration, and vascular proliferation. Both the tachyzoites and encysted bradyzoites may be found at the periphery of necrotic foci. The organisms are usually seen by routine H& E and Giemsa stains, but can be readily recognized by immunocytochemical methods.)
Pneumocystis jiroveci (Pneumocystic jiroveci (formerly called [P. carinii] pneumonia (PCP) is one of the leading causes of death in AIDS patients. The immunocompromised status in AIDS results in opportunistic infections like PCP. The patient presents with dry cough and shortness of breath. Chest X ray shows diffuse bilateral infiltrates extending from the perihilar region. Ground glass appearance is often used to describe chest x-rays in PCP. About 90% of HIV-infected patients with PCP have an elevated LDH. Bronchoalveolar lavage may also prove useful in diagnosis. Other organs may also be affected; hepatomegaly, cotton wool spots, thyromegaly, skin lesions, and bone marrow necrosis have been reported. Treatment is effected with Trimethoprim and Sulfmethoxazole (TMP-SMX). Pentamidine is used in cases with TMP-SMX toxicity. However, relapses are common.

Toxoplasma gondii is an intracellular parasite with predominant nervous system manifestations. Patients usually present with convulsions, disorientation, and dementia.
Cryptosporidium parvum is a diarrhea-causing protozoan in HIV infected patients. Patients present with 20 to 40 episodes of watery stools per day and abdominal cramps.
Coccidioides immitis is endemic to the Lower Sonoran Life valley (SW USA) and is an opportunistic fungal pathogen, particularly for HIV-positive individuals. This organism causes a pneumonia after inhalation of the infective arthrospore. The radiograph results are not consistent with C. immitis.
Histoplasma capsulatum is a dimorphic fungus that is often found in patients with HIV. It has an endemic area in the Ohio and Mississippi River Valley. Usually, biopsy indicates the presence of small, intracellular yeasts.)
Pasteurella multocida (Among the listed zoonotic pathogens , Pasteurella multocida is the only bacterium possessing the described characteristics of the isolate. The bacterium is part of the normal flora of cats, dogs, and other domestic and pet animals. Human infection often follows bite, scratches, or licks from these carrier animals. Increased carriage rates have been observed in cats. Infections following cat bites and scratches are more common. Majority of infections involves skin and subcutaneous tissue. Rapid onset of wound infection and development of cellulitis or abscess at the site of the bite is very characteristic. P.multocida can also cause bacteremia, meningitis, pneumonia, septic arthritis, and osteomyelitis, endocarditis, peritonitis, sinusitis, and urinary tract infection. Persons in extremes of age and immunocompromised individuals, including those with liver cirrhosis, renal disease, hematological malignancies, and post-transplant patients, are at the risk of more severe invasive disease by P.multocida.

Bartonella henselae, the agent of 'cat scratch disease' (CSD), is a fastidious Gram-negative bacterium, and cultural isolation on chocolate agar requires a minimum of 3 weeks of incubation. It gives negative catalase, oxidase, and carbohydrate utilization tests. CSD is often self-limited. Typical clinical presentation is fever and lymphadenopathy developing about 2 weeks after contact with a cat. B.henselae is associated with bacillary angiomatosis also.

Ehrlichia chaffeensis causes human monocyte ehrlichiosis and is transmitted by ticks. E.caffeensis and Coxiella burnetii, the organism of Q fever, are strictly intracellular and fail to grow on cell-free media. C.burnetii is transmitted among animals by ticks. Humans acquire infection mostly by inhalation of contaminated aerosols and also by drinking unpasteurized milk.

Leptospira interrogans is a spirochete that is transmitted by contaminated water/soil and enters humns via mucosal abrasions. It enters the blood spread and causes flu-like symptoms and potophobia. It can develop into aseptic meningitis and in severe cases, vasculitis with hemorrhagic complications.)
Bartonella henselae The boy's history of 'cat scratch', typical presentation with regional lymphadenitis, and the features of the zoonotic infection described are suggestive of Cat Scratch Disease (CSD). The infection is endemic in the U.S. and about 24,000 people have CSD annually, 80% of whom are children. The main agent of CSD is Bartonella henselae. B.henselae is a zoonotic pathogen capable of causing a broad range of clinical manifestations in humans. CSD is usually a self-limited infection in immunocompetent children. Other manifestations of B.henselae infection include bacillary angiomatosis-peliosis, bacteraemia, encephalitis, endocarditis, and neuroretinitis. Bacillary angiomatosis-peliosis is characterized by the formation of vasoproliferative tumors resulting from bacterial colonization and activation of human endothelial cells. Ability to induce endothelial cell proliferation is a common characteristic of Bartonella species pathogenic to humans. Systemic diseases mostly occur in immunocompromised persons. B.henselae is a very fastidious bacterium. Once isolated from the lymph nodes of CSD patients, it needs prolonged incubation in enriched blood media in the presence of carbon dioxide, so detection is often unsuccessful.

The most common form of anthrax caused by Bacillus anthracis is cutaneous anthrax and the lesion on the skin is called a black eschar due to malignant pustules. This organism is a Gram-positive, spore-forming bacillus.

Francisella tularensis is also a pleomorphic Gram-negative, pleomorphic coccobacillus that requires cystiene in the culture media in order to grow. It is typically acquired by humans by contact with infected rabbits or by tickes, lice, or mites. Infection with this organism causes ulcers to develop and eventually caseating granulomas and regional lymphadenopathy.

Brucella melitensis is also a Gram-negative, pleomorphic coccobacillus but it is typically acquired by the ingestion of contaminated food products or direct skin contact. In the latter case, caseating granulomas and abscess formation can occur in the reticuloenthothelial system. However, the most common clinical presentation in humans is undulating fever.

Borrelia borgdorferi is a spirochete that cannot be cultured in vitro. Infection with this organism can cause a spreading annular red lesion often termed a "bulls-eye" rash.)
Rickettsia rickettsii (Rickettsia rickettsii is a rickettsia that causes Rocky Mountain spotted fever. It is transmitted to humans by the wood tick (Dermacentor andersoni) and the dog tick (Dermacentor variabilis.). Typical symptoms include flu appearing 5 to 7 days after the inoculation and a rash (pink macules) that begins in palms and soles, disseminating to the rest of the body and disappearing with pressure. Later on ulceration and ecchymosis can be seen. The neurologic and circulatory systems can also be involved. Treatment is with tetracycline, doxycycline, and chloramphenicol.

Borrelia burgdorferi is a spirochete transmitted to humans by a deer tick (Ixodes scapularis). It causes Lyme disease. There are 3 stages of this disease:
Stage 1 (early localized): usually the first 10 days after the bite. It is a localized erythematous macule or papule, pale in the center (erythema migrans), present at the site of the bite, accompanied by flu-like symptoms.
Stage 2 (early disseminated): A few weeks later. Usually neurological symptoms such as facial nerve palsy or meningitis, and cardiac symptoms as arrhythmias or pericarditis are seen.
Stage 3 (late chronic disease): Developing even years later with symptoms like arthritis, dermatitis, and cardiomegaly.
The diagnosis is mainly clinical. The treatment depends on the severity and the stage of the disease. Doxycycline is used in early stages.

Francisella tularensis is a Gram negative rod that causes tularemia (rabbit fever). It is transmitted to humans by ticks (A. americanum, D. variabilis, and D. Anderson) or flies but also by eating uncooked infected meat, contaminated water, or through skin lesions when skinning rabbits that are infected. The ulceroglandular manifestation is most common. Symptoms such as flu appear 3 to 5 days after the inoculation and depending on the source of infection the patient can also show skin ulcers, pneumonia, pericarditis, and regional lymphadenopathy. The diagnosis is done by serology, but a PCR of the ulcer is also available. Although a vaccine has been around for 50 years, its use has not yet been approved. The treatment is streptomycin and gentamicin.

P. multocida typically does not cause a rash.

Brucella is a group of bacteria found in animals such as dogs, goats, sheep, cattle, deer, or pigs. Humans get infected (Brucellosis) when they come in contact with the animals or their products (milk). Brucellosis can produce abscesses in many different organs such as liver and spleen. The treatment depends on the type of presentation.)
Coxiella burnetii (Q fever is an acute illness that is caused by the Rickettsia Coxiella burnetii. It is transmitted to humans from exposure to infected livestock. The symptoms that this male experienced are consistent with Q fever: fever, chills, headache, muscle pain, and malaise. Endocarditis can be a complication of Q fever.

Brucella is a non-motile gram-negative rod. They do not form spores. The disease caused by Brucella is called Brucellosis. Brucellosis can be caused by Brucella suis, Brucella abortus, Brucella melitensis, and Brucella canis. Malta is where Brucellosis infection was originally documented. Therefore, brucellosis is sometimes called Malta fever. Brucella abortus is not the cause of Q fever. Brucella abortus is one of the causes of brucellosis. Brucella abortus generally infects cattle and it can then be transmitted to humans. Brucella suis is not the cause of Q fever. Brucella suis is one of the causes of brucellosis. Brucella suis generally infects pigs and it can then be transmitted to humans.

Borrelia burgdorferi is not the cause of Q fever. Borrelia burgdorferi is the cause of Lyme disease. This is transmitted to humans by a tick bite, specifically by deer ticks (Ixodes ticks). Borrelia burgdorferi is classified as a spirochete. Some of the symptoms that can be seen with Lyme disease include arthritis, bull's eye rash and fatigue, chills and fever, headache, and muscle pain.

Rickettsia prowazekii is not the cause of Q fever. Rickettsia prowazekii is the cause of epidemic typhus. This is transmitted to humans by the human body louse. War, poverty, crowding, famine, and unsanitary conditions predispose to the occurrence of epidemic typhus. Some of the symptoms of epidemic typhus include rash, headache, chills, delirium, and high fever.)
Bacillus anthracis (Bacillus anthracis is the bacterium isolated. The skin lesion is likely to be acquired as a result of infection from animal products. The gram positive large encapsulated bacilli demonstrated in smear from the lesion, its rapid aerobic growth, characteristic appearance of the colonies, absence of motility, and sensitivity to penicillin support presumptive identification as Bacillus anthracis. The organism is an aerobic spore-bearer that produces a poly-gamma-d-glutamic acid capsule in vivo. The capsule is anti-phagocytic and protects the bacteria from complement-mediated lysis. Spores are highly resistant and are not produced in living tissue. Carbon dioxide levels within the body inhibit sporulation. Exposure to free oxygen is necessary for formation of spores. Absence of motility and absence of hemolysis in culture help to differentiate the organism from other bacillus species often encountered as contaminants in culture. Bacillus anthracis causes three clinical forms of anthrax, cutaneous, inhalational and gastrointestinal. Cutaneous form is the most common. Inhalational anthrax is the most severe form. Complications like septicemia and meningitis can occur. The development and appearance of the skin lesion in the patient is characteristic of cutaneous anthrax (malignant pustule). Anthrax vaccine for humans contains the protective antigen. B. anthracis considered an important agent of bioterrorism because of its virulence factors and physical properties.

Bacillus cereus is an aerobic spore-forming bacillus related to B. anthracis and is a ubiquitous organism. It is motile and produces hemolysis on sheep blood agar. It produces beta lactamase and is therefore resistant to penicillin and other beta lactam antibiotics. It causes food poisoning: emetic type following consumption of preformed toxin in rice dishes and diarrheal type following consumption of contaminated meat or dairy products. B. cereus can also cause severe diseases when combined with predisposing factors in the patient, such as drug addiction, immunosuppression, and prosthetic implants. Endophthalmitis, osteomyelitis, pneumonia, and endocarditis are examples of severe infections. Clostridium perfringens is a large Gram-positive, nonmotile, anaerobic spore-bearing bacillus. It causes invasive infections, myonecrosis, and gas gangrene, often following wound contamination. C. tetani is also a large Gram-positive motile, anaerobic spore-bearing bacillus. It causes tetanus or lockjaw when the spores are injected into the skin. Listeria monocytogenes is a large, Gram-positive, non-spore-forming motile bacillus. It causes food poisoning and meningitis.)
Aerosolized bacteria can be easily inhaled
(The disease is tularemia caused by F. tularensis and the correct answer is 3. The bacterial agents considered Category A bioterrorism agents are the zoonotic pathogens Bacillus anthracis, Yersinia pestis, and Francisella tularensis. They cause anthrax, plague, and tularema, respectively. All possess high infectivity, and the infective dose is very low. 3) Inhalation of a very small number of aerosolized organisms by humans can result in fatal pneumonia and septicemia.

Factors associated with pathogenicity of F.tularensis include its lipopolysaccharide (LPS), surface capsule, and genes in the Pathogenicity Island. 1) They are not spore formers. The unique features that account for increased virulence of F.tularensis subspecies tularensis (type A) are not well understood. Type A infections are predominant in North America and type B in Europe and Asia. F.tularensis does not possess the other properties listed. 4) Not only ticks, but other arthropods like biting flies and mosquitoes, are also vectors for the organism but vectors would not be employed for a bioterrorism attack. The bacterium does not require X and V factors for growth. 2) No secreted toxin has been detected for F.tularensis. 5) The organism is susceptible to aminoglycosides. Gentamicin and streptomycin are drugs of choice for treatment of tularemia, especially in severe illness. F.tularensis produces beta-lactamase. Beta-lactam antibiotics, including third generation cephalosporins, are not effective against the bacterium. Doxycycline and quinolones are useful in less serious disease. Clinical presentation of tularemia depends on the route of entry of the organisms. In addition to arthropod bite, transmission can occur also by direct contact with infected animals or animal tissue, inhalation of aerosols, or ingestion of contaminated food or water. Ulceroglandular, pulmonary, oculoglandular, oropharyngeal, gastrointestinal, and typhoidal are different clinical forms of tularemia. 3) Airborne and waterborne outbreaks and laboratory infections have been reported and aerosolization of the bacteria would be the mode of transmission in an attack of bioterrorism.

Bacillus anthracis is a large Gram-positive bacterium and can be excluded by its morphology. Yersinia pestis may morphologically simulate Francisella tularensis, though its typical morphology shows bipolar staining. Bubonic plague caused by Y.pestis may clinically simulate ulceroglandular tularemia caused by F.tularensis. Y.pestis is transmited by rat flea, not by tick. Ticks are important vectors of F.tularensis. The patient's illness is related to tick bite, and the clinical presentation is in accordance with ulceroglandular tularemia. Therefore, it can be concluded that the isolate is a strain of Francisella tularensis.)