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Brock Biology of Microorganisms

Twelfth Edition

Madigan / Martinko Dunlap / Clark

Chapter 35
Vectorborne and Soilborne Microbial Diseases
Lectures by Buchan & LeCleir
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I. Animal-Transmitted Diseases

35.1 Rabies Bovine Spongiform Encephalopathies aka Mad Cow 35.2 Hantavirus Syndrome

Francisella
Brucella

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I. Animal-Transmitted Diseases
Zoonosis
An animal disease that is transmissible to humans Generally transmitted via direct contact, aerosols, or bites

Diseases in animals may be either


Enzootic: present endemically in certain populations Epizootic: with incidences reaching epidemic proportions

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35.1 Rabies
Rabies
Occurs primarily as an epizootic disease in animals but
can be spread as a zoonotic disease to humans Some reservoirs in the U.S. are skunks, coyotes, and bats Over 50,000 people die annually, primarily in developing countries Over 1,000,000 people receive post-exposure prophylactic care each year
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Rabies

Epidemiology
Widespread in wild animals
5,000 cases reported annually in United States

Skunks, raccoons and bats considered chief reservoir


Almost all human cases due to contact with infected bats

Zero to 4 reported cases in U.S annually


Only 25% have history of dog bite Long incubation period of virus make history unreliable

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Rabies
Causative agent
Rabies virus
Member of rhabdovirus family Sticking bullet shape Enveloped, single-stranded RNA genome

Pathogenesis
Mode of transmission primarily via saliva of rabid animal
Usually due to bite or abrasion Can be contacted via inhalation

Virus multiples in muscle cells at site of infection Virus reaches brain via infected nerve
Virus multiplies extensively in brain Negri bodies form at sites of replication

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35.1 Rabies
Rhabdovirus
A negative-strand RNA virus that causes rabies Infects cells in the central nervous system in most warm-blooded animals Leads to death if not treated Enters the body through a wound or bite In humans, 9 months may pass before onset of symptoms Virus proliferates in the brain and leads to fever, excitation, dilation of the pupils, excessive salivation, and anxiety, fear of swallowing

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35.1 Rabies
Rabies is diagnosed in the lab using tissue samples

Victim of a bite can be treated by passively immunizing with


rabies immune globulin
Also is immunized using a rabies virus vaccine

Rabies spread is prevented largely through immunization Rabies treatment strategy has been extremely successful in

the U.S.
Less than 3 cases a year are reported

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Rabies Virus

Figure 35.2

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Guidelines for Treating Possible Exposure to Rabies Virus

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Transmissible Spongiform Encephalopathies


Symptoms
Early symptoms
Vague behavioral changes Anxiety Insomnia Fatigue

These symptoms progress weeks to months to hallmark symptoms


Muscle jerks Lack of coordination Dementia Deteriorating intellectual function Impaired judgment Memory loss

Disease often progresses to death within a year


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Transmissible Spongiform Encephalopathies


Causative agent
Proteinaceous infectious particles
a.k.a prions Appear to be new class of infectious agent
Differ from bacteria, viruses and viroids

Main characteristics
Increase in quantity during incubation period Resist inactivation via UV and ionizing radiation Resist inactivation by formaldehyde and heat Not readily destroyed by proteases Not destroyed by nucleases Much smaller than smallest virus Composed of protein coded by normal cellular gene
Modified after transcription
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Transmissible Spongiform Encephalopathies


Prevention and Treatment Prions inactivated by autoclaving in 1N NaOH No treatment All forms are fatal

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35.2 Hantavirus Syndrome


Hantaviruses
Cause several severe diseases including
Hantavirus pulmonary syndrome (HPS) and hemorrhagic fever with renal syndrome (HFRS) Both syndromes caused by hantavirus transmission from infected rodents

Named for Hantaan, Korea, where the virus was first recognized for being a human pathogen Significant outbreaks have occurred in the U.S.
Arizona, Colorado, and New Mexico in 1993

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35.2 Hantavirus Syndrome


The genus hantavirus is a member of the Bunyaviridae, a family of enveloped segmented negative-strand RNA viruses Related to hemorrhagic fever viruses such as Lassa fever and Ebola Infections are handled with BSL-4 safety precautions

Infect various rodents including mice, rats, voles, and lemmings


Up to 200,000 cases are recognized annually Most commonly transmitted by inhalation of virus-contaminated rodent excretia
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35.2 Hantavirus Syndrome


Hantavirus Pulmonary Syndrome (HPS)
Characterized by a sudden onset of fever, myalgia,
thrombocytopenia, leukocytosis, and pulmonary capillary leakage Death occurs within several days in 35% of cases No virus-specific treatment or vaccine for hantaviruses

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Tularemia (Rabbit Fever)


Causative agent
Francisella tularensis
Non-motile, aerobic, Gram (-) rod

Pathogenesis
Causes ulcer at entry sight Lymphatic vessels carry organism to regional lymph nodes
Become large, tender and filled with pus

Spread to other body sites via lymphatics and blood vessels Pneumonia occurs in 10% -15% of lung infections
Mortality rate as high as 30%

Multiplies within phagocytes Cell mediated immunity responsible for ridding infection
90% of infected individuals survive in the absence of treatment

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Tularemia (Rabbit Fever)

Epidemiology Occurs among wild animals in Northern Hemisphere In eastern U.S. most infections occur in winter Result from skinning hunted rabbits In western U.S. infections increase in summer Due to bites from fleas and ticks Other reservoirs for infection include Muskrats, beavers, squirrels, and deer
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Tularemia (Rabbit Fever)


Prevention and Treatment Uses of Rubber gloves and goggles when working with animal carcasses Insect repellents and protective clothing

Inspect routinely for ticks after exposure


Vaccine available for workers at higher risk of exposure Treated with gentimicin

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Brucellosis (Undulant Fever)


Causative agent Four varieties of genus Brucella cause disease in humans All fall into a single species Brucella melitensis Traditionally each variety given own species name depending on preferred host B. abortus cattle B. canis dogs B. melitensis goats B. suis pigs Organism is Gram (-) rod

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Brucellosis (Undulant Fever)


Epidemiology Chronic infection of domestic animals Generally involving the mammary gland and uterus Causes contaminated milk and abortions

Abortion not a feature of human disease


Occurs in workers in meat packing industry

Major problem in animals used for food

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Brucellosis (Undulant Fever)

Prevention and Treatment Pasteurization most important control measure Inspection of domestic animals Protective eyewear and gloves when working with animals or animal carcass Attenuated vaccine controls disease in domestic animals Tetracycline combined with rifampin used for treatment Treatment usually given for 6 weeks

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II. Arthropod-Transmitted Diseases


35.3 Rickettsial Diseases

35.4 Lyme Disease


35.5 Malaria 35.6 West Nile Virus 35.7 Plague

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35.3 Rickettsial Diseases


Rickettsias are small bacteria that have strict intracellular existence in vertebrates
Associated at some point with blood-sucking arthropods Three groups: 1) Typhus group, 2) Spotted fever group, and 3) Ehrlichiosis group Named for Howard Ricketts Closely related to human mitochondria

Contain minimal sets of genes required for intracellular


dependency

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35.3 Rickettsial Diseases


Typhus Group
Transmitted by the common body or head louse bite that gets contaminated with louse feces

Spotted Fever Group


Transmitted by dog and wood ticks among others Over 1,000 people acquire the disease every year

Ehrlichiosis Group
Emerging diseases in this group are HGA and HME, which are spread by tick bites

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35.3 Rickettsial Diseases

Prompt recognition of these diseases is essential, but remains difficult Treatment with antibiotics is usually successful Avoiding hosts or using insect repellants are your best bet for reducing your chances of exposure

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The Human Louse, Pediculus humanus

Figure 35.4

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Rocky Mountain Spotted Fever in the United States

Figure 35.5

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Cells of Rickettsia rickettsii

Figure 35.6a-b

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Rocky Mountain Spotted Fever Rash on the Feet

Figure 35.6c

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Ehrlichia chaffeensis, the Causative Agent of HME

Figure 35.7

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35.4 Lyme Disease


Lyme Disease
An emerging tickborne disease that affects humans and other

animals
Named for Old Lyme, CT, where cases were first recognized Most prevalent tickborne disease in the U.S.

Caused by the spirochete Borrelia burgdorferi


Spread primarily by the deer tick Deer and white-footed field mouse are the prime mammalian

reservoirs
Also identified in Europe and Asia

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Lyme Disease

Disease recognized in mid 1970s in Lyme Connecticut

First identified by Dr. Willy Burgdorfer, Univ of Wisconsin

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Lyme Disease
Causative Agent
Bacterium called Borrelia burgdorferi Large microaerophilic spirochete

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Lyme Disease
Epidemiology Disease is zoonotic - transmitted by ticks

Several tick species implicated as vectors


Most important is black-legged tick, Ixodes scapularis Nymph stage actively seeks blood meal, therefore mainly responsible for transmitting disease

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Lyme Disease
Symptoms First Stage Characterized by erythema migrans (skin rash) and enlargement of lymph nodes Rash begins as small red spot at the site of a tick bite and slowly enlarges

Other symptoms influenza-like and include malaise, chills,


fever, headache, stiff neck, joint and muscle pain and backache
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Lyme Disease
Symptoms
Second Stage
Begin 2 to 8 weeks post rash Involve heart and nervous system
Electrical conduction to heart is impaired
Nervous system involvement leads to paralysis of facial muscles and impaired concentration and emotional instability

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Lyme Disease
Symptoms
Third Stage
Characterized by arthritis
Ususally of the large joints such as the knee

Symptoms develop in 60% of untreated cases


Begin within 6 months after rash Slowly disappear over years

Chronic nervous system impairment may occur

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Lyme Disease

Pathogenesis Bacteria introduced into skin through bite of infected tick Once in skin, bacteria migrate outward in radial fashion Cause inflammatory reaction in the skin Migration and inflammation produces an expanding rash Host immunity is initially suppressed Allows for continued multiplication of bacteria Bacteria enter bloodstream and circulate to other parts of the body Bacteria do not cross the placenta

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Lyme Disease
Prevention and Treatment Prevention measures same as Rocky Mountain Spotted Fever Antibiotics relatively effective in early stage disease Less effective in late disease

Presumably because bacteria are not actively


multiplying

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35.4 Lyme Disease


Symptoms of Lyme disease include headache, backache, chills, and fatigue In 75% of cases a large rash occurs at the site of the tick bite

During the initial stages it can be treated with antibiotics


Chronic stage develops in weeks to months
40-60% of these patients develop arthritis Others develop neurological damage or damage to the heart No toxins or virulence factors have yet been identified

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SEM of the Lyme Spirochete Borrelia burgdorferi

Figure 35.8

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Deer Ticks, the Major Vectors of Lyme Disease

Figure 35.9

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Lyme Disease in the United States in 2005

Figure 35.10a

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Reported Cases of Lyme Disease in the U.S. by Year

Figure 35.10b

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Lyme Disease Infection

Figure 35.11

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35.5 Malaria
Malaria
A protist disease caused by Plasmodium spp. Has a complex life cycle that includes Anopheles mosquitos as vectors

Estimates of 350,000,000 people infected worldwide


Each year over 1,000,000 people die from malaria Generally found in tropical and subtropical regions Conclusive diagnosis requires identification of Plasmodiuminfected erythrocytes in blood smears

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35.5 Malaria
Prophylaxis for travel to endemic areas is recommended

Drugs can be used to prevent and treat infections


Malaria may recur years after the primary infection About 1,500 cases in the U.S. annually Several vaccines are currently in development Some individuals in regions that are endemic to malaria

have sickle cell trait and other thalassemias that make


them resistant to malaria

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Malaria
Symptoms Includes fever, headache and pain in the joints and muscles Generally begin 2 weeks post infection Transmission via bite of infected mosquito Symptom pattern changes after 2 to 3 weeks Fall into three categories Cold phase abruptly feels cold and develops shaking Hot phase follows cold phase Temperature rises steeply reaching 104F Wet phase follows hot phase temperature falls and drenching sweat occurs
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Malaria
Causative agent
Human malaria caused by four species of protozoan Plasmodium
P. vivax, P. falciparum, P. malatiae, P. ovale

Infectious form of parasite injected via mosquito

Carried by bloodstream to liver (exo-erythrocytic phase)


Infects cells of liver
Thousands of offspring released to produce infection in erythrocytes

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Plasmodium life cycle

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Malaria
Epidemiology Once common in both temperate and tropical areas Now disease of tropical & sub-tropical lattitides Eliminated from continental U.S.

in late 1940s
Mosquitoes of genus Anopheles are biological vectors Infected mosquitoes and humans constitute reservoir

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Malaria
Prevention and Treatment Treatment is complicated Due to different stages of mosquito life cycle Chloroquine

Effective against erythrocyte stage


Will not cure liver infection

Primaquine and tafenoquine


Generally effective against exoerythrocyte stage and certain species gametocytes
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Life Cycle Plasmodium vivax

Figure 35.12

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Plasmodium falciparum

Figure 35.13

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35.7 West Nile Virus


West Nile fever caused by West Nile Virus (WNV)
Transmitted by mosquito bites
Transmission of WNV is seasonal No antiviral drugs are effective in-vivo against WNV

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A Mosquito, A West Nile Virus Vector

Figure 35.14a

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An Electron Micrograph of the West Nile Virus

Figure 35.14b

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Reported Cases of West Nile Virus in the U.S. in 2006

Figure 35.15a

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Incidence of the West Nile Virus in the U.S. in 2006

Figure 35.15b

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35.7 Plague
Pandemic plague has caused more human deaths than any other infectious disease except for malaria and tuberculosis
Caused by Yersinia pestis, a gram-negative facultatively aerobic rod-shaped bacterium Disease of domestic and wild rodents Humans are accidental hosts and are not critical for maintenance of the disease

Fleas are intermediate hosts and vectors that spread plague


between mammalian hosts

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35.7 Plague
Most cases in the U.S. occur in the southwestern states Y. pestis produces virulence factors that contribute to the disease process Plague is also called bubonic plague because of the

development of buboes in the infected individual


Plague can be successfully treated if it is rapidly diagnosed
Treatment with gentamycin or streptomycin It treatment is started promptly, mortality is only 1-5% of those infected

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Plague Doctor

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Plague (Black Death)


Causative agent
Yersinia pestis
Facultative GNR in Enterobacteriaceae Facultative intracellular bacteria Resemble safety pin in stained preparation (bi-polar staining)

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Plague (Black Death)


Pathogenesis
Masses of organism obstruct digestive tract of rat fleas Flea regurgitates infected material into bite wound Organisms multiply within macrophages Macrophages die and release organism Inflammation in nodes results in characteristic swelling
Nodes become necrotic and spill organisms
Septicemic plague

Mortality rate of untreated reaches between 50% and 80%

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Plague (Black Death)


Symptoms
Develop abruptly 1 6 days post infection
Transmission via bite from infected flea

Disease characterized by large tender lymph nodes called

buboes (Bubonic plague)


Infection in the lung (Pneumonic plague) Untreated, the bacteria spread via the bloodstream producing endotoxic shock & DIC (Septicemic plague)

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Plague (Black Death)

Epidemiology Endemic on burrowing rodent populations in all continents except Australia Prairie dogs, chipmunks, gophers, rock squirrels and their fleas are main reservoir Endemic in rodent reservoir in SW US

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Plague (Black Death)

Prevention and Treatment Prevention directed by rat control Killed vaccine gives short-term partial protection Treatment via tetracycline for some exposed individuals to control epidemics

Gentimicin, ciprofloxacin and doxycycline effective on disease if


given early

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Yersinia pestis, Causative Agent of Plague in Humans

Figure 35.16a

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Plague in Humans: A Bubo Formed in the Groin

Figure 35.16b

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Gangrene and Sloughing of Skin in Hand of Plague Victim

Figure 35.16c

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The Epidemiology of Plague Due to Yersinia pestis

Figure 35.17

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III. Soilborne Diseases

35.8 Fungal Diseases 35.9 Tetanus

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35.8 Fungal Diseases


Only about 50 fungal species cause disease Fungi cause disease through three major mechanisms
Allergic responses to fungi

Production and activity of mycotoxins (i.e., aflotoxins)


Infections (mycoses)
Superficial Subcutaneous Systemic
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35.8 Fungal Diseases

Fungal infections can be especially serious in individuals with impaired immune systems (i.e., AIDS patients) or those taking immunosuppressive drugs

Chemotherapy against systemic fungal infections is


difficult because antibiotics that inhibit fungi also tend to inhibit their hosts

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Typical Forms of Pathogenic Fungi

Yeast

Moulds
Figure 35.18

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Fungal Infections: Athletes Foot and Sporotrichosis

Figure 35.20

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Some Pathogenic Fungi and the Diseases They Cause

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Cryptococcosis
Cryptococcus neoformans - Encapsulated budding yeast

Cryptococcus gattii

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Coccidiomycosis aka Valley Fever


Symptoms
Flu-like symptoms including
Fever, cough, chest pain, loss of
appetite and weight

Causative Agent
Coccidioides immitis
Dimorphic fungus
Mold form grows in soil
Hyphae develop barrel-shaped

Other less common symptoms

include
Formation of tender nodules and pain in joints

arthrospores
Spores become airborne

Most recover spontaneously


Small percentage develop chronic disease

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Coccidiomycosis

Pathogenesis
Arthrospores enter lung through inhalation
Develop into thick-walled spores
Spores mature and rupture

Tissue injury and symptoms mostly caused by immune responses


Organism usually eliminated by host immunity

Small percentage of individuals suffer tissue necrosis Rarely, organisms can be carried out through circulation to other parts of the body
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Coccidiomycosis

Epidemiology Grows only in semi-arid climates Calif central valley, SE Calif, AZ, NM, TX Infections occur only in hot, dry dusty, seasons Dust stirred up by earthquakes can lead to epidemics Rainfall promotes growth of fungus This produces increased numbers of spores Infection can occur by traveling through endemic areas

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Coccidiomycosis
Prevention and Treatment Prevention directed to avoidance of dust endemic areas Watering and planting aid in dust control Rx includes amphotericin B and fluconazole

Treatment is prolonged
Antifungals cause troublesome side effects

Disseminated disease can reactivate

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Histoplasmosis

Symptoms
Most infections asymptomatic Symptomatic disease demonstrates
Fever, cough, chest pain, shortness of breath, mouth sores

Causative Agent
Histoplasma capsulatum
Dimorphic fungus Prefers to grow in soils contaminated with bird and bat droppings Yeast form grown in human macrophages Mold form produces spores
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Histoplasmosis
Pathogenesis Infectious conidia are inhaled with dust Develop yeast form in lung Granulomas form in infected lung tissue

Resemble tubercles of tuberculosis


Granuloma lesions replaced by scar tissue

Some calcify
In underlying immunodeficiency disease spreads throughout body
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Histoplasmosis
Epidemiology
Disease occurs in tropical areas and temperate zones Cave explorers and spelunkers at highest risk Most cases in United States occur in Mississippi and Ohio River drainage and in South Atlantic states

Prevention and Treatment


No proven prevention other than avoiding contaminated areas

Treatment is with amphotericin B and itraconazole used in most


severe cases
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35.9 Tetanus
Tetanus is a serious, often life-threatening disease
Caused by an exotoxin produced by Clostridium tetani Natural reservoir is soils C. tetani gain access to the body through a soilcontaminated wound

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35.9 Tetanus
Tetanus is a serious, often life-threatening disease
Result of C. tetani infection on people is lockjaw, resulting from a rigid paralysis or contraction of the muscles Rx is antitoxin to neutralize exotoxin

Tetanus is preventable, the existing vaccine is

completely effective
Inadequately immunized individuals are at risk

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A Soldier Dying from Tetanus

Figure 35.21

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