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Chapter 3 Bacterial zoonoses.

STREPTOCOCCAL INFECTIONS

Overview

Bacteria in the Streptococcus genus are a diverse group that are all gram-positive spheres arranged in pairs or chains. The name Streptococcus was given to this group of bacteria in 1874 by Theodor Billroth, a Viennese surgeon, because of the bacterium's spherical chain morphology (streptos is Greek for twisted chain and kokkos is Greek for kernel or berry). There are numerous species of Streptococcus bacteria that cause a variety of diseases including strep throat (Str. pyogenes), scarlet fever (Str. pyogenes), and pneumococcal pneumonia (Str. pneumoniae) in humans and strangles in horses (Str. equi), pneumonia in pigs (Str. suis), and mastitis in cattle (Str. agalactiae). In humans Streptococcus bacteria has caused many epidemics throughout history. The first recorded epidemic of scarlet fever, a sequela of strep throat, occurred in Sicily in 1543 and deadly epidemics occurred across the United States from the 1830s until the 1880s. Pneumococcal pneumonia caused by Str. pneumoniae is the most common cause of bacterial pneumonia worldwide. Necrotizing fasciitis, a severe skin and tissue infection caused by a strain of Str. pyogenes that emits a flesh-destroying toxin, has been reported in humans since 1994. In animals Streptococcus infections can cause mastitis, polyarthritis, genital infections, gastric disorders, meningitis, septicemia, pneumonia, and abscesses. Of the numerous species of Streptococcus, only a few of them are zoonotic. Because of better understanding of gene sequencing techniques and relationships between members of the Streptococcus genus, nomenclature and taxonomy of this bacterial group has changed and their role in disease transmission and pathogenesis has been clarified.

Causative Agent

Streptococcus bacteria are gram-positive spheres that grow in chains and may appear ovoid under the microscope when grown in broth culture. They are facultative anaerobes and are catalase negative. Species of Streptococcus are differentiated from each other using many techniques based on antibody reactions, hemolysis patterns, cell arrangement, and biochemical tests. Historically, species of Streptococcus have been classified into Lancefield groups, based on a method developed by Rebecca Lancefield in the 1930s. Lancefield grouping differentiates these bacteria based on a cell wall carbohydrate called component C. The antigenic parts of component C are amino sugars and a precipitation test is used to identify which Lancefield group a species of Streptococcus belongs. There are twenty Lancefield serogroups that are designated by capital letters such as group A Streptococcus, group B Streptococcus, and include groups A through H and K through V. There are some streptococcal species that have no Lancefield group antigens and some with newly identified antigens. The use of Lancefield groups is diminishing, but they will be referred to in the literature and in clinical practice. Another method of distinguishing strains of Streptococci is based on their reaction on blood agar. Some strains of Streptococcus produce extracellular enzymes that produce zones of hemolysis (damage to the red blood cells in the blood agar) and the type of hemolysis they produce or do not produce can help in their identification. Some Streptococcus species produce alpha-hemolysis (partial lysis of the red blood cells to produce a greenish discoloration around the colony), beta-hemolysis (complete lysis of the red blood cells producing complete clearing around the colony), or gamma reaction (no change in the red blood cells leaving the agar unchanged and are referred to as nonhemolytic). Currently Streptococci are subdivided into three large groups: pyogenic (where most pathogens reside), oral, and other.
Classification of streptococcal species
has changed over time; in the 1980s
some species moved to new genera
Lactococcus and Enterococcus) and
more new genera were established
Abiotrophia, Granulicatella,
Dolosicoccus, Facklamia, Globicatella, and
Ignavigranum).


Streptococcal spp. have been isolated from a variety of animals and are found widely distributed worldwide in nature and as commensals. There are more than 37 species of Streptococcus with only a few being pathogenic and even less being zoonotic. Strains of Streptococcus that cause disease are summarized in Table 3-8. Strains of Streptococcus that cause zoonotic disease include:

* Str. equi (group C) is a beta-hemolytic bacterium. Str. equi infections contracted from animals are sporadic in humans and are more frequently associated with Str. equi subspecies zooepidemicus (formerly known as Str. zooepidemicus) than Str. equi subspecies equi. Str. equi subspecies equi occurs almost exclusively in equine causing strangles primarily in young animals without prior infection or immunization and is found in the nasopharynx, upper and lower respiratory tract, and the genital mucous membranes of healthy equine and cattle. Str. equi subspecies zooepidemicus is an opportunistic pathogen found in a large spectrum of animal hosts. Str. equi subspecies zooepidemicus causes pneumonia, wound infections, endometritis, arthritis, and mastitis in animals. Animals can be carriers of this bacterium and horses are the animals most commonly affected by this organism.

* Str. suis (groups R, S, and T) is a nonhemolytic pathogenic and commensal bacteria in swine causing epizootic outbreaks of meningitis, septicemia, and arthritis especially in young, growing pigs. There are at least 35 serotypes of Str. suis with type 2 being the most frequently isolated and the one predominantly isolated from humans. Str. suis causes disease more frequently in swine housed in facilities with high animal densities and poor ventilation and is usually introduced into herds by carrier swine with bacteria in their noses or tonsils (there is also evidence of sow-to-pig transmission). The disease in swine is manifested by meningitis, septicemia, paralysis, convulsion, cutaneous erythema, and fever. In humans meningitis and hearing loss (as a result of cranial nerve VIII involvement) are common signs of Str. suis infection.

* Str. canis (Group G) is a beta-hemolytic opportunistic pathogen and is the most important species of Streptococcus in dogs and cats. Str. canis causes otitis media, septicemia in neonates, lymphadenopathy in cervical lymph nodes, polyarthritis, and reproductive tract infections with abortion and mastitis in dogs. In humans Str. canis has been cultured from wound infections and people with bacteremia.

* Str. iniae (no Lancefield grouping) is a beta-hemolytic bacteria found in freshwater fish and dolphins causing abscesses in these animals. There are both virulent and commensal strains of Str. iniae. Str. iniae has been reported to cause cellulitis and systemic infections (meningitis and endocarditis) in humans. Most human infections have been associated with contact with tilapia fish.

* Str. dysgalactiae (groups A, C, G, and L) is a bacterium that is a pathogen and commensal of animals. Str. dysgalactiae subspecies equisimilis is a beta-hemolytic streptococcal species that occurs worldwide particularly in dogs and cats, cattle, pigs, and poultry. Str. dysgalactiae subspecies dysgalactiae is a nonhemolytic species that is nonzoonotic and causes a variety of animal infections including mastitis in cattle.

* Str. porcinus (group E, P, U, V, none or new) is a beta-hemolytic bacterium that has been isolated from swine and has been isolated from the urogenital tract of women. The zoonotic significance of Str. porcinus is unknown.

* Str. bovis group (group D) are nonhemolytic normal flora bacteria of both humans and animals and include the bacteria Str. bovis, Str. equines, Str. gallolyticus, Str. infantarius, Str. pasteurianus, and Str. lutetiensis. Bacteria in this group are found in humans with endocarditis, urinary tract infections, osteomyelitis, and sepsis and their zoonotic significance is uncertain.

* Str. pneumoniae (no Lancefield grouping) are alpha-hemolytic human pathogens that cause pneumonia, otitis media, and meningitis. Str. pneumoniae causes respiratory disease in horses and is a commensal or respiratory pathogen in other animal species including Guinea pigs and rats. There is some evidence of reverse zoonosis with this particular species of Streptococcus. The zoonotic significance of Str. pneumoniae is uncertain.

* viridans Streptococcus group (no Lancefield grouping) are a diverse group of approximately 26 species of bacteria that are alpha-hemolytic. They are commensals of the mouth, gastrointestinal tract, and vagina of healthy humans and can be found in animals. Some species may be zoonotic causing endocarditis and other infections in people (especially neutropenic people). Some names given to bacteria in this group include Str. mitis and Str. sanguis.

* Str. agalactiae (group B Streptococcus) are beta-hemolytic (subtle) and cause mastitis in cattle and neonatal sepsis and meningitis in people; however, human infections are not zoonotic as Str. agalactiae can be part of the normal flora of human genital and gastrointestinal tracts.

* Str. pyogenes (group A Streptococcus) are beta-hemolytic (large zone) and cause strep throat, scarlet fever, streptococcal toxic shock syndrome, and necrotizing fasciitis in people and may be isolated from animals such as dogs, cattle, ducks, and monkeys that serve as occasional reserviors (chain of infection probably is human to animal to human).
Str. pyogenes bacteria are adapted
to humans and have no natural
animal reservoir. Str. pyogenes can
be transmitted to animals (reverse
zoonosis) and animals can retransmit
the infection to humans. Examples of
reverse zoonosis of Str. pyogenes include
humans infecting the bovine udder
causing contamination of raw milk that
caused human outbreaks and family
dogs that carry the bacterium after
family members had strep throat.


Epizootiology and Public Health Significance

Streptococcus spp. are found worldwide in nature and as commensals in animals. Str. equi subspecies zooepidemicus has the largest spectrum of animal hosts with the presence of animal carriers and diseased animals. Str. suis infections are being diagnosed more frequently in humans; however, human cases have not been seen in the United States. Most human Str. iniae infections have occurred in North America. The other species of Streptococcus that cause human disease are found in a variety of animals including dogs, cats, poultry, and fish.

Human infections with Str. equi subspecies zooepidemicus are rare and occur sporadically usually associated with consumption of unpasteurized dairy products. Mortality rates for group C bacteremia (to which Str. equi subspecies zooepidemicus belongs) is about 20% to 30% and for group C meningitis is about 57%. Human infections with Str. suis are rare with fewer than 100 human cases reported to date. Virulent strains of Str. suis are found in pigs in the United States; however, no human cases have been seen in the United States. The mortality rate for Str. suis meningitis is about 7% with common sequelae of deafness and vertigo. Human infection with Str. canis is rare with less than ten documented cases. Str. iniae infections in humans have been seen in people handling live or freshly killed fish and is mainly seen in the elderly.

Str. pyogenes is a common human pathogen that accounts for more than 10 million infections, with approximately 9,000 cases occurring annually in the United States. The mortality rates are 10% to 15% for invasive disease, 20% to 25% for necrotizing fasciitis, and about 45% for streptococcal toxic shock syndrome.

Transmission

Streptococcus bacteria are often normal flora of animals and humans and can be transmitted in a variety of ways. Str. equi subspecies zooepidemicius is spread to humans by direct contact with animals excreting the pathogen in large amounts (contact with purulent discharges or bites), indirect transmission by fomites, aerosols, or by ingestion (consumption of raw milk and dairy products). Str. suis is transmitted to humans by direct contact with pigs and pork usually through nonintact skin or via the conjunctiva, indirect transmission by fomites, ingestion of undercooked pork from infected pigs, or aerosol. Carriers transmit the infection to other pigs by close contact (mainly between weaned pigs). Str. canis is found on the skin and mucosa of dogs and other animals and transmission seems to be via close contact (colonization of open wounds or through bites). Str. iniae transmission appears to be mainly through contact of traumatized skin with live or freshly killed fish or contaminated instruments. Str. dysgalactia subspecies equisimilis and Str. porcinus can be transmitted to people via contact with infected animals or via bites or scratch wounds from infected animals.

Pathogenesis

Streptococcal infections can result in a variety of diseases and their development depends on several factors such as animal species, bacterial species, body system affected, and portal of bacterial entry. Pyogenic Streptococcus bacteria produce pus as part of their pathogenesis. When pyogenic Streptococcus bacteria enter tissue they cause an inflammatory response including vasodilation and invasion of neutrophils. As a result of chemotaxis (chemical signaling by bacteria) neutrophils move toward bacteria and phagocytose them. Following phagocytosis, bacteria may be digested, but some are resistant to enzymes in the neutrophil and will multiply in the neutrophil. Some Streptococcus bacteria will produce toxins that kill the neutrophils and the enzymes released upon death of the neutrophil will cause liquefaction of dead tissue. This liquefied mass becomes thick pus as a result of the large amount of protein from the nuclei of dead cells. Virulence factors vary among species of Streptococcus and include the following:

* Protein M. Some strains have a membrane protein called protein M that inactivates complement and is antiphagocytic.

* Hyaluronic acid capsule. Hyaluronic acid is a natural substance in the body and its presence in a capsule makes phagocytic leukocytes (WBCs) ignore the presence of bacteria with this virulence factor.

* Streptokinases. There are two streptokinase enzymes that break down blood clots allowing bacteria to spread rapidly throughout infected tissue.

* Streptolysins. There are two different, membrane-bound proteins called streptolysins, which lyse erythrocytes (RBCs), leukocytes, and platelets. These proteins interfere with the oxygen-carrying capacity of blood, immunity, and blood clotting. After phagocytosis, some Streptococcus bacteria will release streptolysins into the cytoplasm of the phagocyte, causing the lysosomes to release their contents causing death to the phagocytes and release of bacteria.

* Enzymes. Some species of Streptococcus produce proteases that break down proteins, others produce deoxyribonucleases (DNases) that reduce the viscosity of fluid containing DNA, whereas others produce hyaluronidases that promote the rapid spread of infection.

* Protein adhesin. Some Streptococcus bacteria produce protein adhesin, a protein that causes binding of the cells to epithelial cells allowing bacteria a place to enter the cells.

Clinical Signs in Animals

Streptococcal infection can cause a variety of diseases in animals as listed in Table 3-8 (see p. 198.) The incubation period of each disease varies with the organism causing the disease and can vary from several hours to days. Streptococcus bacteria that cause disease in animals include:

* Str. equi subspecies equi causes strangles in horses and is considered nonzoonotic. Str. equi subspecies equi occurs almost exclusively in equine and is found in the nasopharynx, upper and lower respiratory tract, and the genital mucous membranes of healthy equine and cattle. Str. equi subspecies equi is transmitted through purulent discharges from one animal to another. Affected horses are infectious for at least 4 weeks following onset of disease and carrier animals can exist. The incubation period in horses is 3 to 6 days and signs of strangles include anorexia, fever, inflammation of the upper respiratory mucosa and lymph nodes, followed by mucopurulent nasal discharge and abscessed lymph nodes in the neck region (Figure 3-72). The normal course of strangles is 10 to 14 days. Morbidity can be close to 100% in a naive population although mortality is low. "Bastard strangles" is a term used to describe strangles that has abscesses in other lymph nodes of the body as a result of the animal's inability to confine the disease to the upper respiratory tract. Str. equi subspecies zooepidemicus is a commensal and opportunistic bacterium in horses. Other animal species may be carriers of Str. equi subspecies zooepidemicus. This bacterium causes a wide variety of infections in animals including secondary bacterial infection following viral respiratory infection that mimics strangles (horses), metritis and placentitis leading to abortion (horses), cervical lymphadenitis, pneumonia, and septicemia (Guinea pigs), polyarthritis, bronchopneumonia, diarrhea, endocarditis, and meningitis (monkeys), and mastitis (cattle and goats). Morbidity and mortality rates can be very high with outbreaks of septicemia.

* Str. suis mainly affects pigs, but has been isolated from cattle, sheep, goats, and bison. Although Str. suis can be carried in swine without producing signs of disease, some virulent strains can cause meningitis, arthritis, or subclinical disease in swine (especially suckling pigs). Acute meningitis in growing pigs can have high mortality rates.

* Str. canis is mainly found in dogs, but can also be found in cats, cattle, rats, mink, mice, rabbits, and foxes. Str. canis has been isolated from dogs with skin infections, reproductive tract infections, mastitis, pneumonia, and septicemica and in cats with arthritis, wound infections, cervical lymphadenitis, pneumonia, and septicemia.

* Str. iniae has been found in freshwater dolphins and wild and farmed fish (tilapia fish can be carriers of this organism). Most fish do not show clinical signs of disease but some fish have exhibited signs of meningoencephalitis and panophthalmitis.

* Str. dysgalactiae subspecies equisimilis produces a variety of clinical diseases in animals including dogs and cats (causing skin infections and respiratory infections), cattle (causing mastitis), pigs (septicemia, arthritis, and meningitis), and poultry (nasopharyngeal infections).

[FIGURE 3-72 OMITTED]

Clinical Signs in Humans

Streptococcal infections in humans vary with the species of bacteria causing the disease. The incubation periods can range from less than 24 hours to approximately 2 to 3 days. Streptococcus that cause disease in people from potential animal sources include:

* Str. equi subspecies zooepidemicus has been isolated from people with pneumonia, arthritis, meningitis, septicemia, glomerulonephritis, and streptococcal toxic shock syndrome.

* Str. suis has mainly been linked to meningitis in people that results in some degree of hearing loss in approximately 50% of infected individuals.

* Str. canis rarely causes human disease but may cause septicemia, meningitis, and peritonitis in people.

* Str. iniae can rarely cause cellulites (Figure 3-73), arthritis, endocarditis, meningitis, and osteomyelitis in people.

* Str. dysgalactiae subspecies equisimilis causes human infections mainly from direct contact with rodents and can cause skin infections, septicemia, endocarditis, and thrombophlebitis.

* Str. bovis group bacteria are found in humans with endocarditis, urinary tract infections, osteomyelitis, and sepsis.

* Str. porcinus has been isolated from the urogenital tract of women.

* Str. pneumoniae causes pneumonia, meningitis, otitis media, and sinusitis in people. Pneumococcal disease is highest in children and the elderly.

* viridians Streptococcus group can cause purulent abdominal infections, dental caries, and endocarditis in people, but typically does not cause human disease.

* Str. pyogenes is a reverse zoonotic agent that can cause pharyngitis (strep throat), abscesses, pneumonia, septicemia, necrotizing fasciitis (flesh-eating bacteria), rheumatic fever, glomerulonephritis, and scarlet fever.

[FIGURE 3-73 OMITTED]

Diagnosis in Animals

Samples obtained from biopsies, smears, or aspirates from wounds, pharyngeal secretions, blood, CSF, or other sites that demonstrate gram-positive cocci in pairs or chains can lead to a presumptive diagnosis of streptococcal infection. Gross lesions produced vary with the species of Streptococcus causing the infection. Str. equi subspecies zooepidemicus typically produce mucus with respiratory infections and abortions with placentitis (in horses the placenta is edematous with brown fibronecrotic exudates and the fetus may be severely necrotic). Lesions in pigs with Str. suis include patchy erythema of the skin, enlarged lymph nodes, and thickened joint capsules. Fish with Str. iniae infection can show exudative meningitis and diffuse visceral hemorrhages.

Diagnosis of Streptococcus is made via culture and identification of the bacteria based on their hemolysis pattern on blood agar, colony morphology, biochemical reactions, and serology to detect antigens. Streptococcus spp. grow on blood agar plate producing pinpoint colonies with varying hemolytic patterns that are species dependent. Streptococcus spp. do not grow on MacConkey agar, but will grow on gram-positive selective agar such as CNA (Columbia agar with colistin and nalidixic acid) and PEA (phenylethyl alcohol agar). Various species of Streptococcus can be identified using biochemical tests such as hippurate and CAMP tests (positive for Str. agalactiae), PYR reaction and susceptibility to bacitracin (positive for Str. pyogenes), and bile solubility and susceptibility to Optochin (positive and inhibition of growth for Str. pneumoniae).

Lancefield group identification can be done using the capillary precipitation test, but other serologic methods can also be used. ELISA tests can also be used to rapidly identify some species of Streptococcus.

Diagnosis in Humans

Diagnosis in humans is similar to that described for animals. Additional serology is sometimes performed to diagnose human streptococcal disease and may include tests like the antistreptolysin O (ASO) titer to determine poststreptococcal sequealea, antihyaluronidaste titer, and anti-DNase B.

Treatment in Animals

Treatment of Streptococcus bacteria in animals typically involves penicillin in which resistance to this antibiotic are uncommon. Other antibiotics that have been used to treat streptococcal infections include tetracyclines and sulfa antibiotics. Carrier animals may or may not be treated.

Treatment in Humans

Streptococcus infections in humans are typically treated with a variety of antibiotics such as penicillin, amoxicillin, ampicillin, cephalosporins, vancomycin, and clindamycin. In cases of shock (usually seen with streptococcal toxic shock syndrome and necrotizing fasciitis), supportive treatment such as IV fluid administration, IV immunoglobulin treatment, and surgical debridement may be warranted. Dialysis may be necessary in cases of glomerulonephritis.

Management and Control in Animals

It is difficult to prevent some Streptococcus bacterial infections because these bacteria are part of the normal flora in some species. Poor husbandry and stress predispose animals to streptococcal infections so good hygiene practices can reduce the risk of these infections. Good hygiene practices during milking can .reduce the risk of foodborne spread of Streptococcus spp. All in/all out management of swine can be helpful in reducing Str. suis in a herd. Conditions such as adding sick animals to a healthy colony or naive animals should also be avoided. If outbreaks occur in animal colonies (such as with Guinea pigs) depopulation of the facility may be warranted. There are no commercial vaccines for Str. equi subspecies zooepidemicus; however, autogenous vaccines for have been used in Guinea pigs. Killed vaccines are available for Str. suis.

Management and Control in Humans

Most Streptococcal infections are transmitted through wounds and abrasions, so the use of protective clothing and gloves are valuable in controlling the spread of this bacterium from animals to people. To prevent foodborne infections the consumption of raw milk and unpasteurized milk products should be avoided. Good hygiene practices when caring for horses with respiratory disease can help decrease the spread of Str. equi subspecies zooepidemicus infections.

Summary

Streptococcus spp. are gram-positive bacteria that occur in pairs or chains. Many species are pathogenic for humans and animals and a few are zoonotic. Clinical identification of Streptococcus bacteria is based on their hemolytic reactions on blood agar and Lancefield grouping. Zoonotic species of Streptococcus include Str. equi subspecies zooepidemicus (formerly known as Streptococcus zooepidemicus), Str. suis, Str. canis, Str. iniae, and Str. dysgalactiae subspecies equisimilis. Str. porcinus, Str. bovis group, Str. pneumoniae, and viridans Streptococcus group have uncertain zoonotic potential. Streptococcus bacteria are often normal flora of animals and humans and can be transmitted in a variety of ways including direct and indirect contact. Streptococcal diseases in animals range from respiratory infection to septicemia to meningitis and range from meningitis to pharyngitis to pneumonia to endocarditis in people. Diagnosis of streptococcal infections includes Gram stain reaction and morphology, growth and hemolysis pattern on culture, biochemical tests, and antigenic testing. Treatment of streptococcal infection includes antibiotics and in cases of shock supportive care. Streptococcal infections can be controlled with proper hygiene practices for animals and people. Avoidance of ingestion of unpasteurized dairy products can also limit the risk of acquiring streptococcal infections.

TUBERCULOSIS

Overview

Tuberculosis, also known as consumption, is so named because of the characteristic tiny nodule (tubercle) resulting from infection by Mycobacterium spp. Tuberculosis (TB) has been present in human and animal populations since antiquity (Egyptian mummies from 2400 B.C. show pathologic lesions of TB) and was known as phthisis (Greek for wasting or decay) or consumption because of the way the disease consumed the infected individual. In 460 B.C. Hippocrates named phthisis as the most prevalent disease of the day killing nearly everyone it infected. The lesions produced in patients with TB were first called tubercles in 1689 by Dr. Richard Morton, a London physician. Treatment, diagnosis, and prevention of TB have changed with a variety of scientific discoveries. Treatment of TB changed when Hermann Brehmer in 1854 advised that a TB patient be moved to a healthier climate, which resulted in curing this patient's disease and the beginning of sanatorium construction for TB patients. In 1882, Robert Koch discovered a staining technique that allowed him to visualize My. tuberculosis and gave hope that a cure would be forthcoming. Wilhelm Konrad von Roentgen's 1895 discovery of radiation allowed physicians to monitor the progression of TB through chest x-rays. French bacteriologist Calmette, together with Guerin, used special culture media to lower the virulence of My. bovis, creating the basis for the BCG (Bacille Calmette Guerin) vaccine for people still in use today. Antibiotic treatment for TB became available in the middle of World War II (1943) when streptomycin was found to be effective at treating TB infections. Despite all of the efforts aimed at understanding and treating TB, it remains the leading killer of people among all infectious diseases. Famous people who contracted and died of TB include King Tutankhamen, John Keats, FrEdEric Chopin, Edgar Allan Poe, Eleanor Roosevelt, and Vivien Leigh. Nelson Mandela contracted TB, but did not die from the disease.

Causative Agent

Mycobacterium spp. are gram-positive (though weakly staining), acid-fast bacilli that are nonendospore forming, obligate aerobes that have an unusual waxy cell wall that affects many of its properties, including its slow growth (doubling time is 20 hours compared with 20 minutes with other bacteria) and staining ability (Figure 3-74). This waxy cell wall allows it to survive prolonged periods of drying and also affects its acid-fast staining property. The waxy cell wall also contains mycolic acid components that protect the bacterium from lytic enzymes and oxidants within phagocytes. One mycolic acid is called cord factor, which causes the bacterium to clump into cordlike masses that adds to the organism's virulence (strains of Mycobacterium without cord factor are avirulent). Cord factor also inhibits migration of neutrophils and is toxic to mammalian cells. There are three main types of tubercle bacilli recognized: human (My. tuberculosis), bovine (My. bovis), and avian (My. avium) with the two mammalian species (tuberculosis and bovis) being more closely related. My. tuberculosis along with My. bovis, My. africanum, and My. microti all cause the disease known as tuberculosis and are members of the tuberculosis complex; however, My. tuberculosis is usually pathogenic for primates (including humans), whereas My. bovis is pathogenic for animals. The types of Mycobacterium differ in their characteristics in culture media and pathogenicity and may produce infection in host species other than their own.

* My. tuberculosis infects humans and other nonhuman primates. Humans are the ultimate reservoir for My. tuberculosis. This species will occasionally infect dogs and parrots, but is mainly found and spread in primates. Cattle infected with My. tuberculosis can cause false-positive skin test results for My. bovis, but are not clinically sick. Pigs may be infected with My. tuberculosis by eating table scraps from the household of an infected person (leads to granulomas in the gastrointestinal tract and regional lymph nodes). Dogs infected with My. tuberculosis can develop granulomas in many parts of the body including the pharynx where it can be transmitted to other animals and people. Birds can develop cutaneous granulomas from My. tuberculosis.

* My. bovis can produce disease in most warm-blooded vertebrates including humans. This organism is the principle agent of zoonotic tuberculosis.

* My. avium is the only species found in birds, but can also infect swine, cattle, sheep, mink, dogs, cats, and cold-blooded animals. My. avium is found in soil and water (perhaps the real reservoir in zoonotic transmission) and can cause disease in humans and both domestic and wild animals. My. avium complex (MAC) consists of 2 species: My. avium and My. intracellulare that cause disseminated infection mainly in people with immune system compromise secondary to AIDS and immunosuppressive chemotherapy.

* My. marinum, My. fortuitum, My. platypolcitis, My. scrofulaceum, My. kansasii, and My. intracellulare have been reported in a variety of animals and may be present in soil and water.

* My. africanum is a cause of human tuberculosis in tropical Africa and its retention as a distinct species is probably not warranted.

* My. microti causes tuberculosis in voles, wood mice, shrews, llamas, badgers, ferrets, cattle, pigs, and cats.

[FIGURE 3-74 OMITTED]

Epizootiology and Public Health Significance

TB affects nearly all species of vertebrate animals and at one time was one of the major diseases of humans and domestic animals. My. tuberculosis has been reported in some animals, but infections are often traced to infected humans who expose susceptible animals to infection. My. bovis is found in susceptible animals such as ungulates, carnivores, primates (including humans), lagomorphs, and rodents. Several wildlife reservoir hosts have also been identified including whitetailed deer, opossums, and badgers.

WHO estimates that 3 million people die from TB annually and 8 million people are infected with the disease (95% of cases are in developing countries). The registered number of new TB cases worldwide correlates with economic conditions with the highest incidence of TB found in Africa, Asia, and Latin America (countries with the lowest gross national product). In industrialized countries, the incidence of TB was in decline until the mid-1980s when cases of TB began increasing. This rise in tuberculosis cases was attributed to high rates of immigration from TB-ravaged countries and HIV infection. The resurgence of TB can also be attributed to multiple drug-resistant strains of Mycobacterium; causing physicians to use antibiotic combination therapy to ensure that the bacilli are killed during the treatment.

Transmission

Animals contract Mycobacterium infections primarily via the respiratory and gastrointestinal tracts. Respiratory transmission (inhalation of contaminated aerosols or fomites) is the most efficient type of TB transmission. Animals or humans with active TB produce respiratory droplets that contain one to three organisms and these TB-containing droplets can remain suspended in air for several hours. Infection occurs when an infected animal coughs and inhalation of the contaminated droplet reaches the alveoli of the lung. Indirect transmission via contaminated feed, pasture, or water (contaminated by mucus secretions, feces, urine, or milk with infective organisms) is another important route of transmission. Other less frequent routes of transmission include bites, vertical transmission (which may actually result from aerosol transmission from parent to offspring in close quarters), and direct contact from infected animals grooming healthy animals. The route of infection determines the disease manifestations of TB. Aerosol spread leads to involvement of the lungs and thoracic lymph nodes; ingestion of contaminated food and water results in involvement of the lymph tissues associated with the intestinal tract.
Overcrowding, poor sanitation,
malnutrition, and lack of disease
knowledge have all contributed
to problems with treating and
preventing the spread of TB.


Humans contract TB by the respiratory tract (aerosol transmission of droplets or inhalation of dust), gastrointestinal tract (consumption of uncooked meat or unpasteurized milk from TB-infected animals), or integumentary system (direct injury to skin and mucous membranes). One of the main reasons people pushed for pasteurization of milk was to eliminate TB organisms in milk and dairy products. Transmission of Mycobacterium is summarized in Figures 3-75A and 3-75B.

Pathogenesis

Tubercular infection typically begins with inhalation of infective respiratory droplets containing the tubercle bacilli. The inoculum of bacteria is usually no more than three organisms, which are engulfed by alveolar macrophages, but not killed. The bacilli continue to multiply slowly inside and outside host cells. From the alveolar macrophages the organisms may be carried from the primary focus to the regional lymph nodes and spread via lymph and blood to multiple organs (most of these disseminated lesions heal). Lymphatic drainage from the primary focus leads to the formation of caseous (dry and crumbly) lesions in an adjacent lymph node. The primary focus and the lymph node lesion are called the primary complex. The primary complex seldom heals.
My. bovis can survive for about 4 days
on fomites and several months on feces
or in animal carcasses; however, its
survival in the environment is reduced
by drying, exposure to sunlight, and
high temperature.


Several weeks later, cell-mediated immunity is activated and T lymphocytes stimulated by mycobacterial antigens begin to proliferate and secrete lymphokines. The immune response also stimulates tuberculin hypersensitivity; a form of type IV delayed hypersensitivity, which causes the reactive tuberculin test used in diagnosis of TB.

When bacteria localize in an area, they stimulate the formation of tumor-like masses called tubercles. The tubercle is an inflammatory lesion produced when the activated macrophages engulf the bacteria and isolate them. The tubercle contains a few phagocytized mycobacteria surrounded by many activated macrophages and lymphocytes. These viable bacteria can continue to multiply causing the tubercles to enlarge. As the tubercles increase in size, the host cells often die within the tubercle and the dead tissue looks caseous (cheesy). A few bacteria can survive in the caseous center and remain viable for many years. The caseous masses have a tendency to undergo mineralization (calcification), liquefaction, or may become enclosed by dense, fibrous connective tissue and the disease becomes inactive. Reactivation of the infection can occur months or years later if the immune response is weakened. Bacteria can escape from the primary site and travel via the lymphatic and vascular systems to other organs where they establish other tubercles. If the vascular system contains numerous organisms from a local lesion, many tubercles develop in major organs such as the lungs causing a rapidly fatal disease (this acute, generalized infection is called miliary tuberculosis, named after the small lesions that form that resemble millet seeds). If small numbers of organisms enter the circulation from a primary complex a few isolated lesions develop in other organs, become encapsulated, remain small for long periods of time, and do not cause clinical signs of disease. The time it takes to develop clinical TB depends upon the interaction of the host's immune response and proliferation of bacteria in macrophages. Tubercule formation is illustrated in Figure 3-76.

[FIGURE 3-75A OMITTED]

[FIGURE 3-75B OMITTED]

[FIGURE 3-76 OMITTED]

Clinical Signs in Animals

Clinical signs of TB depend on the extent and location of the lesions. General signs of TB include weakness, anorexia, dyspnea, emaciation, and low-grade fever. When lungs are extensively involved there may be an intermittent, hacking cough. Species specific signs include:

* Cattle. Acute TB lesions are usually found in the thorax and occasionally lymph nodes causing the classical signs of wasting, weakness, anorexia, and dyspnea. In advanced stages of TB lesions may be found in many organs including the udder, uterus, kidneys, and meninges (Figure 3-77). Skeletal muscles are seldom affected.

* Swine. Swine can be infected with My. tuberculosis, My. bovis, and My. avium, which are usually contracted by ingestion. The clinical signs of TB in swine are associated with the gastrointestinal tract and regional lymph nodes. Swine infected with My. bovis typically have rapidly progressive disease with caseation of lesions.

* Sheep and goats. TB is rare in sheep and goats. When infected with My. bovis the disease in sheep and goats is similar to that of cattle; when infected with My. avium the disease causes disseminated lesions.

* Dogs. TB lesions in dogs usually resemble neoplasms (especially carcinomas). Lesions are typically found in the lungs, pleura, and liver. The lesions appear differently depending on the area involved varying from ones with depressed centers and hemorrhagic edges (liver) to ones containing liquid.

* Cats. Cats are resistant to My. tuberculosis infection, but may become infected with My. bovis by ingestions of contaminated milk. TB lesions in cats are found primarily in the gastrointestinal tract; however, respiratory infection and contaminated wounds can also be infection sources.

* Nonhuman primates. Monkeys and apes are susceptible to My. bovis, My. tuberculosis, and My. avium. Signs of TB in nonhuman primates include behavioral changes, anorexia, lethargy, and sudden death while appearing to be in good condition. Depending on the organ system involved other signs may include diarrhea, skin ulceration, splenomegaly, and hepatomegaly.

* Poultry. The digestive tract is the entry site of My. avium with predominant lesions found in the liver, spleen, intestine, and bone marrow. Poultry TB is common on small rural farms where poultry has been housed for many years in contaminated housing. TB is less common in commercial poultry operations as a result of rapid turnover of animals.

* Equine. Horses, donkeys, and mules are less susceptible to TB than bovine and the lesions seen in these animals usually involve the gastrointestinal tract. Tubercles in equine are rarely caseous or calcified.

[FIGURE 3-77 OMITTED]

Clinical Signs in Humans

TB in people is a multifaceted disease. Primary TB typically is asymptomatic and may only be recognized by the development of a positive skin test. People who develop clinical signs of TB are typically homeless or alcoholic people, immunosuppressed people, the elderly, nursing home residents, and people suffering from such diseases as diabetes mellitus and lymphoma. The incubation period is from 4 to 6 weeks. Clinical signs of TB in humans depend on the organ system involved. Signs of pulmonary TB include cough, production of sputum, and hemoptysis (coughing up blood) (Figure 3-78). Regional lymph nodes are affected but heal and develop calcifications. As pulmonary TB progresses people may develop a subfebrile temperature, night sweats, lymphadenopathy, fatigue, anorexia, and erythema of the extremities. The clinical signs of cutaneous TB are highly variable and may show ulcerated, nodular, or hemorrhagic skin lesions, which spread superficially or extend to deeper skin layers. Generalized or extrapulmonary TB may affect almost any organ system, but typically affects the lymph nodes, pleura, genitourinary tract, skeletal system, meninges, and peritoneum. Clinical signs of extrapulmonary TB include anorexia, weight loss, fatigue, high and sustained fever, night sweats, and chills; however, the patient may be asymptomatic for years. Bone and joint TB mainly affects the hip and stifle regions with clinical signs of pain, swelling, and decreased range of motion. Destruction of vertebrae with damage to the spinal cord is a sequela of spinal TB (also known as Pott's disease).

[FIGURE 3-78 OMITTED]
The principle sign of TB is chronic
wasting or emaciation despite adequate
nutrition and care.

Laryngeal TB is highly infectious because
it can be spread to other people by
talking.


Diagnosis in Animals

Pathologic findings for TB include the tubercle, which microscopically consists of a cluster of macrophages surrounding bacteria. Since the macrophages engulf the bacteria yet do not inhibit their growth, the lesion can be of varying sizes (Figure 3-79). As the bacteria multiply, the nearby cells undergo necrosis, the center may become caseous, and in time the center of the tubercle may calcify (except with My. avium infections). Simple tubercles are approximately between 1 mm and 2 cm in diameter, but large tubercles may be formed when tubercles coalesce with other tubercles. Tubercles in which bacteria are eventually killed may contain fibrous scar tissue. If this does not occur secondary infection with other organisms may occur followed by liquefaction and necrosis of the tubercle producing cavitation.

Grossly, tubercles either in organs or on a surface are firm, pale nodules that contain yellowish, caseous, necrotic centers that are dry (versus pus filled as in an abscess). If calcification has occurred the tubercle has a white gritty appearance. If the tubercle breaks into a blood vessel or large numbers of bacilli are released into the bloodstream, many small tubercles (2 to 3 mm in size) that are the same age and size are seen. These lesions are seen in miliary tuberculosis, so named because the lesions look like a scattering of millet seeds.

Clinical diagnosis of TB can only be done when the disease has reached an advanced state, at which time animals are typically shedding organisms and are an infection source for other animals. Antemortem identification of TB is critical in controlling this disease. The tuberculin skin test is used in animals and is based on the premise that animals infected with Mycobacterium bacteria are allergic to the proteins in the tuberculin and develop delayed-type hypersensitivity reactions when exposed to this protein. The tuberculin is placed intradermally in the deep layers of the skin and in infected animals will elicit a local reaction characterized by inflammation and swelling. The USDA has accepted the tuberculin test for identification of My. bovis in cattle, bison, goats, and captive cervids.

[FIGURE 3-79 OMITTED]

The purified protein derivative (PPD) tuberculin for veterinary use is made from My. bovis and can identify infections caused by My. bovis and My. tuberculosis. A My. avium PPD tuberculin is used when testing for avian tuberculosis because animals infected with My. avium react less to tuberculin made from My. bovis. Most countries use PPD tuberculin at a dose of 0.1 mL (0.1 mg of protein) containing 5,000 tuberculin units in mammals and 0.05 mL containing 2,500 tuberculin units in chickens. The results from PPD tuberculin tests are used to classify animals as negative for infection (response to the test is negative), suspected to have infection (response to the test is unclear), or reactor (response is positive). In the United States, two specific skin tests are used:

* The caudal fold skin test is used for large mammals such as cattle, sheep, goats, and bison and tuberculin is typically injected in one of the folds at the tail base (Figure 3-80A). Swine are injected in the skin behind the ear or vulva. Chickens are injected in the skin of the wattle. The injection sites are observed and palpated 72 hours after injection for cattle, sheep, and goats and 48 hours after infection for swine and chickens. The caudal fold tuberculin test used to be done every three years on cattle; now it is used in cases of transport or sale or during slaughter-suspect cases.

* The comparative cervical tuberculin test is conducted only by regulatory state or federal veterinarians and is performed by injecting My. avium and My. bovis PPD tuberculins into separate sites in the skin of the neck. Both injection sites are then observed and palpated and the difference in size of the two responses allows for the differentiation of infection by My. bovis versus My. avium, My. avium subspecies paratuberculosis, or transient saprophytic mycobacteria found in the environment. The comparative cervical tuberculin test has greatly reduced the incidence of reactors without gross lesions (decreased the number of false positives). This test is not used in herds where My. bovis has been diagnosed.
Nonhuman primates should be tested
with tuberculins prepared for veterinary
use as the tuberculins prepared
for human use are not of sufficient
potency to elicit the delayed-type
hypersensitivity response in these
species. Eyelids are used as injection
sites as they can be viewed from a
distance (used in zoos).


Animals that test positive or suspect are removed from the farm and examined postmortem for confirmation of mycobacterial infection. Microscopy with acid-fast stains can detect acid-fast bacilli in tissue samples. Bacterial culture using LowensteinJensen agar is still required to confirm a diagnosis of TB; however, this can take 6 to 8 weeks. PCR techniques have been developed for the diagnosis of My. tuberculosis and My. bovis. DNA fingerprinting techniques have also been developed and are helpful in identifying potential sources of infection or relatedness of strains.

Diagnosis in Humans

Clinical symptoms, especially in high risk individuals, along with laboratory testing are used to diagnose TB in humans. Chest radiographs are not pathognomonic since any pattern of infiltrate can be seen. Samples of sputum, bronchial secretions, gastric secretions, CSF, body fluids, and biopsies are used for microscopy, culture, and molecular methods of detected Mycobacterium infections. A tissue sample obtained surgically or at necropsy show acid-fast bacilli within tubercles and is sufficient to establish a diagnosis of TB. Final confirmation is based on bacterial culture. Microscopy with acid fast stains can detect acid-fast bacilli; however, culture is mandatory for identification and can take several weeks. Culture media for Mycobacterium spp. include Lowenstein-Jensen agar and Middlebrook 7H10 and 7H11 agar. Automated systems may also be used. ELISA testing is also available; however, results should be verified by culture and histopathology. PCR can detect less than 10 bacteria, but should not replace culture.

[FIGURE 3-80 OMITTED]

Tuberculin skin testing is also used in humans and indicates past exposure to My. tuberculosis and some cross-reactivity with other mycobacteria. The preferred skin test for My. tuberculosis infection is the intradermal or Mendel-Mantoux method (Figure 3-80B). Five tuberculin units of PPD in 0.1 mL of solution is injected intradermally into the volar surface of the forearm. Tests are read after 48 to 72 hours and the transverse diameter (in mm) of induration (hardened mass) is recorded. Three cutoff levels are used for defining a positive test ([greater than or equal to] 5, [greater than or equal to] 10, and [greater than or equal to] 15). The cutoff used depends on the health status of the individual (immunosuppressed people with chest lesions are read at the low range, whereas people with no known risk are read at the high range). In some individuals (those without a known prior-positive skin test, have not had a tuberculin skin test within a 1-year period, and have an initial negative skin test) it is recommended to have a two-step PPD test to detect individuals with past TB infection who now have diminished skin test reactivity. The two-step PPD test involves performing the first skin test (which turns out negative) and repeating the skin test 7 days after the initial one. The second test is read in 48 to 72 hours after its placement. If the second test shows a positive response, it may demonstrate a boosted response to an old infection (in time the antibody levels from a previous infection become too low to detect with the one-step test). Boosting can last up to 2 years; therefore, the two-step test reduces the likelihood that repeated skin testing might falsely indicate new infection. People with positive skin tests then have chest radiographs taken as well as sputum samples for culture.

Treatment in Animals

The antituberculosis drug, isonicotinic acid hydrazide (INH) or isoniazid, can treat bovine TB; however, the disadvantages to treatment in animals include emergence of drug-resistant strains, excretion of antibiotic in milk and meat, and relapse when therapy is discontinued making treatment of TB impractical.

Treatment in Humans

People are treated with a variety of antibiotics; however, isoniazid has the highest antibacterial activity for Mycobacterium bacteria and inhibits the development of resistance making it the treatment of choice. Treatment typically lasts 9 months with isoniazid (other drugs are given for a shorter amount of time). Isoniazid is hepatotoxic and liver enzymes are monitored during treatment. Some strains of My. tuberculosis are extremely drug-resistant (XDR) making treatment difficult.

Management and Control in Animals

In 1917, the Cooperative State-Federal Tuberculosis Eradication Program, administered by the USDA Animal and Plant Health Inspection Service (APHIS), state animal health agencies, and United States livestock producers, was initiated because TB caused more losses among U.S. farm animals in the early part of the 1900s than all other infectious diseases combined. This program has nearly eradicated bovine TB from the U.S. livestock population and has reduced human disease. Initially, all cattle herds were systematically tested, and all reactors were slaughtered. Premises were cleaned and disinfected after infected cattle were removed. As a result of this program, the reactor rate in U.S. cattle was reduced from 5% to approximately 0.02%.

Control programs for TB currently revolve around four components:

* Prevention. TB prevention focuses on reducing exposure to the pathogen and reducing the likelihood that an exposed animal will become infected after exposure. Cattle are mainly infected by infected cattle that reside on the farm or are introduced into the herd. If livestock in a herd are tested for TB and are negative, maintaining a closed herd is the best way to prevent TB on a farm. Basic hygiene practices and biosecurity practices (routine testing and quarantine of imported animals, manure management, and maintenance of feed and water) have reduced the risks of My. bovis spread on cattle farms. Population control in wild reservoir animals has also been necessary as a result of their interaction with cattle. The BCG vaccine does not completely prevent infection in cattle or other animals and as a result of the fact that vaccinated animals will test positive on the tuberculin skin test, the vaccine has not been used in the United States.

* Treatment. The antituberculosis drug INH has made treatment practical for TB; however, the treatment of cattle in the United States and many other countries is forbidden as a result of the shedding of organisms to other animals during treatment and the effects on the eradication program of keeping animals that will test positive for TB in the herd.

* Eradication. In domestic livestock herds, culling of reactors and after a waiting period (12 months in the United States) allowing livestock to repopulate the site. The USDA also allows regulatory agencies to develop herd-specific test-and-slaughter programs for individual livestock operators and managers of wildlife farms (such as deer, elk, and buffalo). Eradication of My. bovis from wildlife reservoirs is more difficult and has included such strategies as trapping and removal programs, directed hunts to reduce animal numbers, restrictions on feeding and baiting animals, or provision incentives to hunters to increase the number of animals harvested during a hunting season.

* Surveillance. Surveillance of TB involves antemortem testing and slaughter surveillance of livestock and captive animal species.

Management and Control in Humans

There are a variety of ways to prevent the spread of TB. One important step to preventing the spread of TB is to isolate and treat all disease carriers until they are no longer an infective risk. The live, attenuated BCG vaccine is used in humans in many foreign countries (it is considered effective in about 80% of vaccinates) and may be recommended in high risk groups. BCG vaccine protects children from miliary TB and TB meningitis. The concern with human vaccination is that vaccinated individuals will have a positive PPD TB test, making surveillance procedures ineffective. If traveling to a country where TB is a concern, people should get vaccinated and avoid people with persistent coughs. Improvement of socioeconomic conditions that can lead to persistent levels of TB within a group (such as prisons, homeless shelters, nursing homes, AIDS victims, and immigrants living in crowded conditions) can greatly reduce TB mortality. Laboratories that may handle Mycobacterium organisms (including performing cultures, identification, and susceptibility testing) are designated as Biosafety level 3 facilities and specific precautions are taken.
A 1994 outbreak of bovine TB infection
in the wild white-tailed deer population
spread into nearby cattle prompting
testing and surveillance of a variety of
wildlife.


Summary

Tuberculosis is a chronic disease in humans and animals caused by My. tuberculosis, My. bovis, and My. avium. Zoonotic TB has been greatly reduced by control and eradication programs in cattle. Animals contract My. bovis infections primarily via the respiratory and gastrointestinal tracts, whereas humans contract TB by the respiratory tract, gastrointestinal tract, or integumentary system. Clinical signs of TB in humans and animals depend on the organ system involved. General signs of TB in animals include weakness, anorexia, dyspnea, emaciation, and low-grade fever. When lungs are extensively involved there may be an intermittent, hacking cough. Clinical presentation of TB in humans includes cough, production of sputum, and hemoptysis (coughing up blood); cutaneous TB lesions are typically ulcerated. Generalized signs of TB include anorexia, weight loss, fatigue, fever, and chills and the patient may be asymptomatic for years. PPD testing is used in both animals and humans to diagnose and control TB. Animals are not treated for TB and are culled from the herd. People are treated with INH for extended periods of time (9 months). Drug-resistant strains of My. tuberculosis have made treatment more difficult. Control programs for TB revolve around prevention, treatment, eradication, and surveillance.

VIBRIOSIS AND CHOLERA

Overview

Vibriosis and cholera, diseases primarily of the gastrointestinal tract, are caused by bacteria in the Vibrio genus. Vibrio comes from the Latin vibrare meaning to quiver and this genus of bacteria moves in an undulating pattern much like quivering. Vibriosis is most commonly caused by Vi. parahemolyticus (which causes diarrhea) or Vi. vulnificus (which causes skin infections and/or septicemia). The diarrhea-causing Vi. parahemolyticus is a relatively harmless infection, but Vi. vulnificus infection can lead to septicemia and death. In 1951, Japanese bacteriologists discovered Vi. parahemolyticus as a cause of illness among people who eat fish from contaminated waters.
In the past, vibriosis was a term used
to describe diseases caused by the
curved bacterium Campylobacter.
Campylobacter bacteria are sexually
transmitted in animals and the
diseases they cause are now called
campylobacteriosis.

The disease hog cholera is caused by an
RNA virus and is not associated with the
diseases caused by Vibrio bacteria.


Cholera, also known as Asiatic Cholera, is a severe bacterial infection of the gastrointestinal tract caused by Vi. cholerae. Cholera was a rare disease confined to India before the 1800s. It became one of the world's first epidemics as the disease broke out in Calcutta in 1817 from contaminated water. The spread of cholera was aided by the Industrial Revolution and the accompanying growth of urban tenements and slums. In the United States, the Industrial Revolution caused immigrants to move into crowded living quarters, which helped cholera spread to a large degree and provided an ongoing source of new infections. Cholera and its effects helped develop the United States infrastructure because most municipal water mains and sewer systems were built in the late 1800s to help contain the disease. Public health agencies were also formed and funded during this time as well as building codes and ordinances.

Dr. John Snow began investigating the spread of cholera during the London epidemics of 1848 and 1849, developing his theory that cholera was waterborne and taken into the body orally. Dr. Snow proved that water used from a common pump had the cholera organisms, whereas private water sources did not. The actual discovery of the comma-shaped bacillus of cholera was made by the German bacteriologist Robert Koch in 1883. Through microscopic examination, he concluded that feces may contain cholera bacteria for a period of time after the actual onset of the disease. All cases of cholera today are part of a pandemic strain (Vi. cholerae 01, biotype El Tor) that started in Indonesia in 1961.

Causative Agent

Vibrio infections are considered foodborne diseases because the majority of these infections are associated with the consumption of contaminated food. Infections caused by Vibrio species are classified into two groups: Vi. cholerae and non-cholera Vibrio (which are further classified as halophilic [need sodium chloride for growth] Vibrio species and nonhalophilic [do not need sodium chloride for growth] Vibrio species). Vibrio spp. are oxidase positive, gram-negative curved bacteria with a single flagellum (Figure 3-81). Vibrio spp. can produce multiple exotoxins and enzymes that are associated with extensive tissue damage that play a major role in disease development.

* Vi. parahemolyticus and Vi. vulnificus are halophilic, noncholera Vibrio found in salt water. Both organisms live in areas where the temperature exceeds 18[degrees]C (in the United States it is found along the coasts that border the Gulf of Mexico, New England, and the northern Pacific coast). Infection with either of these two bacteria primarily occurs through eating contaminated raw seafood such as raw oysters. Both bacteria are ingested by filter-feeding mollusks such as oysters, mussels, clams, and scallops; filter-feeding concentrates bacteria in these mollusks providing a large inoculum of bacteria for the person ingesting them. Vi. parahemolyticus, which has a rapid doubling time of 9 minutes under ideal conditions, causes acute watery diarrhea with abdominal cramps and fever approximately 24 hours after eating shellfish. Vi. vulnificus infection occurs following ingestion of contaminated fish or contact of a wound with seawater or contaminated seafood. Vi. vulnificus causes cellulitis and septicemia. Cellulitis can result in severe tissue destruction leading to amputation in some cases. Infection with Vi. vulnificus can cause death in up to 50% of immunocompromised people who contract it.

* Vi. cholerae is primarily found in humans; however, it can survive in freshwater and seawater. In epidemic areas cholera bacteria are found in contaminated water systems. In areas where public sanitation is adequate, the majority of cholera cases are a result of ingestion of infected shellfish. Vi. cholerae has also been isolated from birds and herbivores, and has experimentally caused disease in dogs, Guinea pigs, and rabbits.
Cholera transmission and onset
of epidemics is influenced by the
season and climate. Cold, acidic, dry
environments inhibit the survival
of Vibrio, whereas warm, monsoon,
alkaline, and saline conditions favor
their survival.


[FIGURE 3-81 OMITTED]

Epizootiology and Public Health Significance

Vibriosis

In the United States, vibriosis is not commonly recognized as a cause of illness, partly because of proper sanitation systems and because clinical laboratories rarely use the culture techniques necessary to identify this organism. In addition, not all states require that Vi. parahemolyticus infections be reported to the state health department (CDC collaborates with the Gulf Coast states of Alabama, Florida, Louisiana, and Texas to monitor the number of cases of Vibrio infection in these regions and the Foodborne Diseases Active Surveillance Network (Food Net) tracks Vi. parahemolyticus in regions outside the Gulf Coast). Most cases of vibriosis in the United States occur in coastal states between June and October. Between 1988 and 1991, there were only 21 reported cases of Vi. parahemolyticus infection in the United States. Between 1988 and 1995, there were over 300 reports of Vi. vulnificus infection in the United States (although it is believed to be underreported). In 1997, the incidence of diagnosed Vi. parahemolyticus infection in the United States was 0.25 per 100,000 people. In Asia, Vi. parahemolyticus is a common cause of foodborne disease.

Since 1988, the CDC has maintained a voluntary surveillance system for culture-confirmed Vibrio infections in Alabama, Florida, Louisiana, Mississippi, and Texas. The estimated illnesses caused by all noncholera Vibrio species in the United States are 8,000 per year resulting in approximately 60 deaths. Vi. parahemolyticus is the most common noncholera Vibrio species reported; however, Vi. vulnificus is associated with 94% of reported deaths. Because clinical laboratories do not routinely use the selective medium thiosulfate-citrate-bile salts-sucrose (TCBS) for stool culture, many cases of Vibrio-associated gastroenteritis are not reported.

In recent years in the United States, the prevalence rate of infections caused by noncholera Vibrio species appears to be increasing. The combination of increased water temperature where shellfish have been harvested and increased salt levels in these bodies of water may have contributed to the increased contamination rate of shellfish. Worldwide, areas such as Japan, Taiwan, China, Hong Kong, and Korea frequently report noncholera Vibrio infections, which may be related to the high prevalence of hepatitis B resulting in liver disease.

Cholera

In the United States, cholera was prevalent in the 1800s but has been rare in industrialized nations for the last 100 years. In industrialized nations cholera has been virtually eliminated through the use of modern sewage and water treatment systems. Improved transportation, however, results in more people from the United States traveling to Latin America, Africa, or Asia where epidemic cholera occurs. U.S. travelers to areas with epidemic cholera may be exposed to the cholera bacterium or may bring contaminated seafood back to the United States. Between 1995 and 1999 there were 53 confirmed cases of cholera in the United States, including one death, caused by the Vi. cholerae 01, biotype El Tor strain. Most of these infections were acquired in other countries; however, four came from eating Gulf Coast seafood.
Cholera was generally thought to be the
scourge of the depraved, poor masses
because these groups tended to be
affected the worst.


Cholera is still common today in some parts of the world, including the Indian subcontinent and sub-Saharan Africa (Figure 3-82). In January 1991, epidemic cholera appeared in South America (Peru) and quickly spread to 21 countries infecting 700,000 people and killing 6,000.

Transmission

Vibriosis

Halophilic Vibrio (Vi. parahemolyticus and Vi. vulnificus) inhabit coastal waters and associate with zooplankton. Halophilic marine organisms such as crustaceans and shellfish contract Vibrio infections primarily by ingesting these zooplankton. Ecologically, Vibrio organisms degrade chitin and recycle the breakdown products.

[FIGURE 3-82 OMITTED]

In temperate zones, Vibrio bacteria survive over winter by settling into the ocean sediment and are resuspended during the warmer seasons. As they are resuspended, they are incorporated into the food chain where they eventually grow on fish, shellfish, and other edible seafood. People contract the disease by ingesting contaminated seafood or through direct contact of an open wound with contaminated seawater. There is no evidence of person-to-person transmission.

Cholera

Cholera can be contracted by drinking water or eating food contaminated with Vi. cholerae. When epidemics occur, the source of the contamination is usually the feces or vomitus of an infected person. The disease can spread rapidly in areas with inadequate treatment of sewage and drinking water. Cholera is often spread by someone who is infected with the bacterium who prepares food for others or by sharing a drinking cup with a healthy individual.

Vi. cholerae can also live in the environment in brackish rivers and coastal waters. Raw shellfish have been a source of cholera, and people in the United States have contracted cholera after eating raw or undercooked shellfish from the Gulf of Mexico. The disease is not spread directly from one person to another.

Pathogenesis

Once Vibrio organisms are ingested with food or water, they enter the stomach where some of the organisms die. Those bacteria that survive the extreme acidity of the stomach penetrate the mucus layer of the duodenum and jejunum using their flagella, adhering to the outside of the epithelium but not penetrating the mucosal cells. The bacteria begin replicating and release toxin that disrupts the normal physiology of the intestinal cells by altering the levels of chemical messengers resulting in removal of anions from the cell through the cell membrane. Depending upon the species of Vibrio and the toxin it produces, the epithelial cells become damaged and secrete large amounts of electrolytes (chloride and bicarbonate ions in particular) into the intestinal lumen. As the cell secretes large amounts of chloride and bicarbonate ions into the intestinal lumen, water follows resulting in massive amounts of fluid loss through the intestines (cholera) or fluid loss that is self-limiting (vibriosis). The chemicals produced by the bacteria can also damage epithelial cells resulting in ulceration of the affected areas. As a result, profuse diarrhea occurs producing stools that resemble water flecked with small particles of mucus known as the rice-water stools of cholera. The loss of water as a result of cholera infection is extensive (up to one liter per hour in humans).
Vibrio bacteria cause disease in humans
by production of toxins and enzymes
rather than invasion of epithelial cells
(the intestinal lining may appear normal
in affected individuals).


Vi. vulnificus causes cellulitis and septicemia following ingestion of shellfish or exposure to sea water. Vi. vulnificus can get through the intestinal wall and into the bloodstream and produces multiple chemicals, such as proteases, hemolysins, and cytolysins, which are associated with its virulence.

Clinical Signs in Animals

Shellfish and other halophilic marine animals do not show clinical signs of disease when infected with Vibrio bacteria.

Clinical Signs in Humans

Vibriosis

Vi. parahemolyticus causes watery diarrhea often with abdominal cramping, nausea, vomiting, headache, fever, and chills. Symptoms typically occur within 24 hours of ingestion and the disease is usually self-limiting lasting for about 3 days (ranges from 2 to 10 days). Severe disease is rare and occurs more commonly in immunocompromised people. Vi. parahemolyticus can also cause a skin infection producing large, fluid-filled blisters on the arms or legs when an open wound is exposed to warm, contaminated seawater.

Vi. vulnificus can cause disease in people who ingest contaminated seafood or water or have an open wound that is exposed to contaminated seawater. Ingestion of Vi. vulnificus can cause vomiting, diarrhea, and abdominal pain in healthy people; however, in immunocompromised people (especially those with chronic liver disease) Vi. vulnificus can result in septicemia, causing a severe and life-threatening illness characterized by fever and chills, decreased blood pressure, and blistering skin lesions. Septicemia from Vi. vulnificus is fatal about 50% of the time. Vi. vulnificus can also cause a skin infection when open wounds are exposed to warm seawater resulting in skin breakdown and ulceration.

Cholera

Clinical signs of cholera in humans appear 1 to 7 days following consumption of contaminated food or water. Abdominal bloating and cramps that quickly progresses to produce large quantities of very watery stool are classic signs of cholera. The stool has little odor and is often referred to as rice-water stool because of its appearance (very watery, light colored, and laced with tiny flecks of mucus but not blood). Typically the person is afebrile and occasionally will be vomiting. People infected with cholera may experience intense thirst, extreme weakness, sunken eyes, decreased urination, dry, wrinkled skin, rapid heart rate, lowered blood pressure, weakened pulse, sleepiness, unconsciousness, seizures, or kidney failure. Death is caused by the dehydration.

Diagnosis in Animals

Diagnosis in animals is not performed other than for surveillance.

Diagnosis in Humans

Vibriosis can be diagnosed via Gram stain and culture from samples of stool, blood, or blister fluid. Cholera can be diagnosed via gram stain and stool culture. For isolation of Vibrio pathogens the use of a selective medium that has thiosulfate, citrate, bile salts, and sucrose (TCBS agar) is recommended (Figure 3-83). These organisms are all oxidase positive and vary in their fermentation properties (lactose versus sucrose) and ability to grow in varying concentrations of sodium chloride (Vi. cholerae cannot grow in salt, Vi. parahemolyticus and Vi. vulnificus cannot grow without salt). Suspicion of Vi. parahemolyticus infection is warranted if a patient has watery diarrhea and has eaten raw or undercooked seafood, especially oysters, or when a wound infection occurs after exposure to contaminated seawater. Vi. vulnificus skin lesions or septicemia may be suspected in immuno-compromised people with skin blisters or ulcerations or signs of blood infection such as fever or shock. Suspicion of Vi. cholerae is warranted if a patient has returned from an endemic country or coastal region where the water or food may be contaminated.

Treatment in Animals

Shellfish and halophilic marine animals are typically not treated. In cultured, aquarium fish and confined fish skin, fins, and tail ulcerations may be treated with sulfamerazine (there is a withdrawl time for fish marketed for human consumption).

Treatment in Humans

Treatment in humans is typically symptomatic including fluids either by mouth or intravenously. Treatment is not necessary in most cases of Vi. parahemolyticus infection and there is no evidence that antibiotic treatment decreases the severity or the length of the illness. Patients should drink plenty of liquids to replace fluids lost through diarrhea.

[FIGURE 3-83 OMITTED]

Vi. vulnificus infections are treated with antibiotics such as tetracycline or doxycycline plus ceftazidime. One out of five patients with vibriosis requires hospitalization.

Cholera is treated with oral rehydration therapy (ORT), which was developed in the 1960s that is cheaper, easier, and more effective than IV fluid replacement. Patients are treated with an oral rehydration solution, a prepackaged mixture of sugar and salts to be mixed with water and drunk in large amounts. This solution is used throughout the world to treat diarrhea. With prompt rehydration therapy, fewer than 1% of cholera patients die. Antibiotics, typically tetracycline, are given to prevent the bacterium from replicating in the intestinal lumen.

Management and Control in Animals

Vi. vulnificus and Vi. parahemolyticus are bacteria naturally present in marine environments and elimination of them from natural water systems is impossible. Contamination with Vibrio bacteria does not clinically affect shellfish and does not change the look, smell, or taste of the seafood. Management of these organisms is based on lowering the risk of disease is people. In the United States oysters can only be harvested legally from waters free from fecal contamination; however, even legally harvested oysters can be contaminated. Voluntary reporting of Vi. vulnificus infections to CDC and to regional offices of the FDA help state officials with tracking of shellfish and sampling of harvest waters to discover possible sources of infection and to close oyster beds when problems are identified.

Management and Control in Humans

Vibriosis can be prevented by avoiding raw or undercooked shellfish, keeping raw shellfish and its juices away from cooked foods (cross-contamination), and avoiding contact of wounded skin with seawater or raw seafood. When an outbreak is traced to an oyster bed, health officials recommend closing the oyster bed until conditions are less favorable for Vi. parahemolyticus. There is no national surveillance system for Vi. vulnificus, but the CDC collaborates with the states of Alabama, Florida, Louisiana, Texas, and Mississippi to monitor the number of cases of Vi. vulnificus infection in the Gulf Coast region.

The risk for cholera is very low in the United States; however, travelers visiting areas with epidemic cholera should only drink water that has been boiled or treated with chlorine or iodine (including tea, coffee, and ice), eat only foods that have been thoroughly cooked and are still hot, eat only fruit that you have peeled yourself, and eat only cooked vegetables. Seafood from these areas should not be brought to the United States. Cholera is a reportable disease in the United States.

The only licensed cholera vaccine in the United States has been discontinued because of the brief and incomplete immunity it provided. Cholera vaccination is not required for entry or exit in any country. Two recently developed vaccines for cholera are licensed and available in other countries and appear to provide better immunity and fewer side-effects than the previously available vaccine.

U.S. and international public health authorities continue to enhance surveillance for cholera, investigate cholera outbreaks, and design and implement preventive measures. The EPA works with water and sewage treatment operators in the United States to prevent contamination of water. The FDA tests imported and domestic shellfish for Vibrio organisms and monitors the safety of U.S. shellfish beds.

Summary

Vibriosis and cholera are diseases caused by Vi. parahemolyticus, Vi. vulnificus, and Vi. cholerae. Cholera, caused by Vi. cholerae, is typically spread person to person, but may be found in contaminated water and aquatic animals. Vi. cholerae produces diarrhea with severe electrolyte imbalances and extreme levels of fluid loss. Cholera is rarely seen in the United States. Cholera is diagnosed via gram stain and stool culture. Cholera is treated with oral rehydration therapy. Vibriosis is typically spread from consumption of contaminated water and shellfish or through skin wounds from contaminated water. Vi. parahemolyticus typically produces a self-limiting gastroenteritis; whereas Vi. vulnificus produces skin lesions and septicemia, which is fatal in about 50% of affected people. Vibriosis can be seen in higher amounts in coastal states as a result of the consumption of undercooked shellfish or contact with contaminated water. In humans, vibriosis can be diagnosed via culture from samples of stool, blood, or blister fluid. Vi. parahemolyticus infections in people are treated with fluid therapy. Vi. vulnificus infections are treated with antibiotics such as tetracycline or doxycycline plus ceftazidime. Vibriosis can be prevented by avoiding raw or undercooked shellfish, keeping raw shellfish and its juices away from cooked foods (cross-contamination), and avoiding contact of wounded skin with seawater or raw seafood. The risk for cholera is very low in the United States; however, travelers visiting areas with epidemic cholera should only drink water that has been boiled or treated with chlorine or iodine, eat only foods that have been thoroughly cooked and are still hot, eat only fruit that you have peeled yourself, eat only cooked vegetables, and should not bring seafood from these areas to the United States.

For a list of less common bacterial zoonoses, see Table 3-9 (p. 224).

Review Questions

Multiple Choice

1. In regard to the taxonomic scheme, what is true?

a. Kingdoms are the smallest and most general taxon in the Linnaean system of classification.

b. Binomial nomenclature uses kingdom, phylum, class, order, family, genus, and species in its naming system.

c. Writing scientific names involves capitalizing the genus name and using a lower case letter to begin the species name.

d. There are seven levels in the Linnaean system arranged in descending ranks with species being the most diverse.

2. Prokaryotic cells

a. usually have a single, circular chromosome located in the nucleoid region of the cell.

b. have chromosomes that are not surrounded by a nuclear membrane.

c. have few organelles in comparison to eukaryotic cells.

d. all of the above.

3. Bacteria are identified by

a. their growth on culture.

b. their Gram stain reaction and morphology (shape).

c. biochemical tests.

d. all of the above.

4. The principle of the Gram stain is based upon the fact that

a. bacteria have different shapes that the stain makes easier to see.

b. some bacteria grow differently on the various types of agars.

c. bacteria may be grouped together in special arrangements.

d. some bacteria have a different cell wall structure than others.

5. Ways that bacteria can cause infection include

a. the presence of flagella that allow bacteria to attach to certain body sites.

b. the presence of a capsule that inhibits chemical identification of the bacterium by phagocytes.

c. the presence of fimbria that help bacteria reach a body site where they can survive and multiply.

d. the presence of normal flora that help foreign bacteria colonize an area of the body.

6. What are true regarding anthrax?

a. Anthrax is primarily a disease of herbivores such as cattle, sheep, goats, and horses.

b. Humans are susceptible to anthrax in industrial (animal-based industry) and nonindustrial (contaminated milk and meat) settings.

c. The pulmonary form is called woolsorter's disease, which is contracted by inhaling endospores during handling of infected animal hair or products.

d. All of the above are true.

7. This organism is most commonly associated with foodborne illness following ingestion of contaminated dairy products. Small numbers of this organism are significant because they can survive and multiply at refrigerator temperatures.

a. Listeria monocytogenes

b. Erysipelothrix rhusiopathiae

c. Bacillus anthracis

d. Pasteurella multocida

8. Erysipelothrix infections in humans characteristically produce

a. CNS pathology.

b. lesions at the point of entry into the host.

c. formation of abscesses in visceral organs.

d. urinary tract pathology.

9. A person develops a nonspecific disease several weeks after receiving a gift of Mexican goat cheese. A gram-negative coccobacilli is isolated from the person's blood culture. Based on this information, what is the most likely organism causing this person's symptoms?

a. Bacillus

b. Streptococcus

c. Pasteurella

d. Brucella

10. A picnic of potato salad, chicken, and hamburgers was consumed during a family reunion on a hot summer day. Within 24 hours ten family members had diarrhea, fever, and abdominal pain. Symptoms lasted for 3 days. Laboratory analysis of stool samples revealed that the organism was gram-negative bacteria and [H.sub.2]S producers that grew on selenite agar with brilliant green. What is the most likely organism?

a. Shigella dysenteriae

b. Salmonella typhimurium

c. Listeria monocytogenes

d. Staphylococcus aureus

11. A miner in the southwestern United States who develops the symptoms of bubonic plaque most likely had contact with

a. rodents.

b. arthropods.

c. wild dogs.

d. dead birds.

12. What bacteria is most likely to cause watery diarrhea?

a. Enterohemorrhagic E. coli

b. Enteropathogenic E. coli

c. Enteroinvasive E. coli

d. Shigella sonnei

13. What bacteria causes strangles in horses and pneumonia in people?

a. Pasteurella multocida

b. Streptococcus equi

c. Burkholderia pseudomallei

d. Staphylococcus aureus

14. Spontaneous abortion in cattle is related to infections with

a. Bacillus abortus.

b. Staphylococcus aureus.

c. Brucella abortus.

d. Streptococcus abortus.

15. A person was admitted to the hospital with a diagnosis of appendicitis. During surgery, the appendix appeared normal and an enlarged lymph node was removed and cultured. Small, gram-negative rods were isolated from the room temperature agar plate. What is most likely to have been involved with this scenario?

a. Shigella sonnei

b. Salmonella enteritidis

c. Escherichia coli

d. Yersinia enterocolitica

16. The bubonic plague is transmitted by the bite of an infected

a. rat.

b. flea.

c. raccoon.

d. mouse.

17. What bacterium is highly communicable because of its low infective dose?

a. Staphylococcus aureus

b. Streptococcus pyogenes

c. Salmonella typhi

d. Shigella spp.

18. A recent immigrant from Africa was seen by his physician because he had developed nodules, abscesses, and ulcers in his oral mucous membranes. A mucopurulent, blood-tinged discharge was seen from these mucous membrane lesions. It was revealed upon staining of the discharge that bacteria were present (gram-negative rods). A definitive diagnosis was done by observing the Straus reaction after inoculating Guinea pigs with some of the material. What organism and disease does this person have?

a. Burkholderia pseudomallei; melioidosis

b. Streptococcus pyogenes, necrotizing fasciitis

c. Staphylococcus aureus, toxic shock syndrome

d. Burkholderia mallei; glanders

19. What bacterium causes wound infections and septicemia in immunocompromised people who have eaten raw or improperly cooked seafood?

a. Vibrio vulnificus

b. Salmonella enteritidis

c. Yersinia pestis

d. Camplyobacter jejuni

20. Travelers to areas of the world where cholera is endemic

a. have no means of prevention.

b. should avoid tick bites.

c. can be immunized against cholera.

d. should wear protective clothing.

21. The botulism toxin induces paralysis in the body by

a. degrading the cell membrane of leukocytes.

b. preventing the release of acetylcholine at the synapse.

c. causing pseudomembranous colitis.

d. altering the normal flora balance of the gastrointestinal tract.

22. What bacterium causes pneumonia in people, air sacculitis in birds, and eye infections in cats?

a. Chlamydophila psittaci

b. Campylobacter jejuni

c. Clostridium tetani

d. Clostridium perfringens

23. The most common transmission route of Mycobacterium tuberculosis in people is

a. ingestion.

b. inhalation.

c. cutaneous.

d. hematologic.

24. What is false in regards to Mycobacterium spp.?

a. acid-fast

b. obligate anaerobe

c. slow replication time

d. high cell wall lipid content

25. What bacteria cause rat-bite fever?

a. Staphylococcus aureus and Streptococcus pyogenes

b. Streptobacillus moniliformis and Spirillum minus

c. Mycobacterium tuberculosis and Mycobacterium leprae

d. Capnocytophaga spp. and Bergeyella zoohelcum

26. The foods most often associated with Clostridium botulinum food poisoning are

a. poultry and eggs.

b. improperly home canned goods.

c. fish and shellfish.

d. poorly cooked pork products.

27. The foods most often associated with Salmonella food poisoning are

a. poultry and eggs.

b. improperly home canned goods.

c. fish and shellfish.

d. poorly cooked pork products.

28. Rice-water stools are characteristic of

a. typhoid fever.

b. dysentery.

c. plague.

d. cholera.

29. A person is admitted to the hospital with fever, chills, and night sweats. Blood cultures were obtained and on the third week grew a gram-negative rod. This patient worked in a pig processing plant. The cultured organism is most likely

a. Pasteurella multocida.

b. Brucella suis.

c. Bacillus anthracis.

d. Capnocytophaga spp.

30. What bacteria can be found in animal bite wounds and can cause snuffles in rabbits?

a. Pasteurella multocida

b. Brucella suis

c. Bacillus anthracis

d. Capnocytophaga spp.

Matching
31. -- Clostridium tetani          A. antibiotic-associated
                                      pseudomembranous colitis
32. -- Clostridium perfringens     B. traveler's diarrhea
33. -- Clostridium difficile       C. hemolytic uremic syndrome
34. -- Enterotoxigenic E. coli     D. pathogen that causes sustained
                                      muscle contraction
35. -- Enteropathogenic E. coli    E. infantile diarrhea
36. -- Capnocytophaga spp.         F. pathogen that causes gas gangrene
37. -- Vibrio parahemolyticus      G. shigellosis-like diarrhea
38. -- Enterohemorrhagic E. coli   H. pyoderma in dogs; boils in people
39. -- Enteroinvasive E. coli      I. woolsorter's disease
40. -- Brucella abortus            J. tuberculosis
41. -- Streptococcus pyogenes      K. shellfish-associated
                                      gastroenteritis
42. -- Burkholderia pseudomallei   L. cat-scratch disease
43. -- Burkholderia mallei         M. ornithosis
44. -- Mycobacterium leprae        N. #1 cause of human gastroenteritis
                                      in United States
45. -- Bartonella henselae         O. tuberculoid and lepromatous
                                      leprosy
46. -- Chlamydophila psittaci      P. glomerulonephritis and
                                      necrotizing fasciitis
47. -- Campylobacter jejuni        Q. pathogen found in dog and cat
                                      bite wounds
48. -- Mycobacterium tuberculosis  R. melioidosis
49. -- Bacillus anthracis          S. glanders
50. -- Staphylococcus aureus       T. undulant fever in people; Bang's
                                      disease in animals


Case Studies

51. A previously healthy 9-year-old girl was awakened during the night by excruciating abdominal pain, nausea, and copious watery diarrhea every 30 to 60 minutes. She was brought into the acute care clinic where she developed bright red bloody diarrhea. She was sent to the emergency room and admitted to the hospital. She had not had contact with any other people with diarrhea and no history of recent travel outside of the United States. Her symptoms appeared 24 hours after eating a hamburger at a local fast-food restaurant. Laboratory work revealed a leukocytosis on the CBC (complete blood count) and a normal UA (urinanalysis). Routine stool cultures were set up in the laboratory.

a. What bacteria could cause foodborne gastrointestinal illness?

b. Is the consumption of hamburger significant in this case history?

c. Because this patient had bloody diarrhea, the stool sample should be cultured on what additional agar?

d. What additional condition should be of a concern in this patient?

52. A 52-year-old male developed severe vomiting and diarrhea during a flight from Bangkok to New York. On landing he was examined at the airport clinic, but left against medical advice. Approximately 12 hours later he went into shock and was brought into an emergency room by family members. This patient spent the next 3 days in the intensive care unit of the hospital. Upon getting a thorough history from him, he remembered that he ate fried fish in Bangkok and sushi on the airplane.

a. Based on this person's history, what bacterium could be making him sick?

b. Why did this person go into shock?

c. What is this bacterium's virulence factor?

d. What is the mechanism of action of this virulence factor?

53. A 22-year-old college student went to his physician complaining of severe abdominal pain and diarrhea. This episode had begun approximately 4 days ago as a mild stomachache that has now developed into intermittent abdominal pain in the lower right quadrant. On physical examination the physician determined the student had abdominal tenderness, normal vital signs, and was afebrile. The student had never traveled outside of the United States and had not consumed raw seafood. Laboratory results revealed a normal CBC and chemistry panel. Stool culture on Salmonella-Shigella and Hektoen enteric agar were negative. An additional culture was done using Skirrow's medium incubated at 42[degrees]C, which produced slow-growing, pinpoint colonies.

a. Based on this person's history and laboratory results, what bacterial infection do you think he has?

b. What are some possible sources of this infection?

c. Is this type of enteritis common in the United States?

54. A 65-year-old man presented to the emergency room with localized chest pain. Past medical history was unremarkable; however, this person's social history included being homeless, a heavy smoker, and a moderate drinker (two to three glasses of wine or beer per day). On physical examination he had poor dental health, clear lungs on auscultation, and pain on deep inspiration.

a. Based on this person's history what might be a cause of his illness?

b. What organism causes this disease?

c. What specimens should be sampled and what test should be run?

d. How is the disease transmitted?

e. Is this infection easy to treat?

55. A 10-year-old boy presented to his physician with an infected dog bite wound. Material from the wound was Gram stained revealing gram-negative rods that exhibited bipolar staining. Culture on blood agar revealed convex, smooth, gray, nonhemolytic colonies. Biochemical tests indicated that this organism was indole positive, urea negative, catalase positive, and ferments mannitol, sucrose, and maltose.

a. What is the most likely cause of this boy's wound contamination?

b. What were the dog's clinical signs of this infection?

c. What else should the physician ask about this case?

References

Abedon, S. 2004. An Introduction to Taxonomy. http://www.mansfield.ohiostate. edu/~sabedon/black09.htm (accessed February 10, 2004).

Alcamo, I. E. 1998. Schaum's Outlines: Microbiology. New York: McGraw-Hill.

Altekruse, S. F., N. J. Stern, P. I. Fields, and D. L. Swerdlow. 1999. Campylobacter jejuni: an emerging foodborne pathogen. Emerging Infectious Diseases 5(1):28-35.

Badshah, C. 2005. Cholera. http://www.nlm.nih.gov/medlineplus/ency/ article/000303.htm (accessed November 30, 2005).

Barrali, R. Jr. 2006. Salmonella infection. http://www.emedicine.com/emerg/ topic515.htm (accessed April 15, 2006).

Bauman, R. 2004. Microbiology. San Francisco, CA: Pearson Benjamin Cummings.

Biddle, W. 2002. A Field Guide to Germs. New York: Anchor Books.

Bronfin, D. 2003. Yersinia enterocolitica infection. http://www.emedicine.com/ ped/topic2465.htm (accessed May 20, 2003).

Bruning-Fann, C. 1998. History of bovine tuberculosis. http://www.michigan.gov/ emergingdiseases/0,1607,7-186-25804_26354-74838--,00.html (accessed May 14, 2005).

Burgess, B. A., P. S. Morley, and D. R. Hyatt. 2004. Salmonella enterica in a teaching hospital. JAVMA 225(9):1344-8.

Burton, R., and P. Engelkirk. 2004. Microbiology for the Health Sciences, 7th ed. Philadelphia, PA: Lippincott, Williams & Wilkins.

Center for Food Security and Public Health. 2005. Listeriosis. http://www.cfsph.iastate.edu/Factsheets/pdfs/listeriosis.pdf (accessed May 1, 2005).

Centers for Disease Control and Prevention. 1998. Rat-bite fever--New Mexico, 1996. Morbidity and Mortality Weekly, Vol 48: No 5. http://www.cdc.gov/ mmwr/preview/mmwrhtml/00051368.htm (accessed December 15, 2004) pp. 89-91.

Centers for Disease Control and Prevention. 2003. Anthrax. http://www.bt.cdc.gov/ agent/anthrax/needtoknow.asp (accessed October 25, 2005).

Centers for Disease Control and Prevention. 2004. General information on Clostridium difficile infections. http://www.cdc.gov/ncidod/dhqp/id_CdiffFAQ_general.html (accessed May 20, 2005).

Centers for Disease Control and Prevention. 2005. Campylobacter infections. http://www.cdc.gov/ncidod/dbmd/ diseaseinfo/campylobacter_g.htm (accessed October 6, 2005).

Centers for Disease Control and Prevention. 2005. Leptospirosis. http://www.cdc.gov/ncidod/dbmd/diseaseinfo/ leptospirosis_g.htm (accessed November 12, 2005).

Centers for Disease Control and Prevention. 2005. Listeriosis. http://www.cdc.gov/ncidod/dbmd/diseaseinfo/ listeriosis_g.htm (accessed February 2006).

Centers for Disease Control and Prevention. 2005. Streptococcus pneumoniae disease. http://www.cdc.gov/ ncidod/dbmd/diseaseinfo/streppneum_t.htm (accessed November 11, 2005).

Centers for Disease Control and Prevention. 2005. Yersiniosis. http://www.cdc.gov/ ncidod/dbmd/diseaseinfo/yersinia_g.htm (accessed March 30, 2005).

Centers for Disease Control and Prevention. 2006. Staphylococcal food poisoning. http://www.cdc.gov/ncidod/ dbmd/diseaseinfo/staphylococcus_food_g.htm (accessed May 29, 2006).

Centers for Disease Control and Prevention Division of Bacterial and Mycotic Diseases. 2005. Melioidosis. http://www.cdc.gov/ncidod/dbmd/diseaseinfo/ melioidosis_g.htm (accessed October 12, 2005).

Chamberlain, N. 2003. Rat-bite fever. http://www.kcom.edu/faculty/chamberlain/ website/lectures/lecture/ratfever.htm (accessed November 27, 2006).

Chamberlain, N. R. 2004. Plague. http://www.kcom.edu/faculty/chamberlain/ website/lectures/lecture/plague.htm (accessed August 3, 2004).

Cliver, D., and M. Hajmeer. 2006. Veterinary Food Safety. http://www.vetmed.ucdavis.edu/PHR/VMD413/2006/41306SYL2.pdf (accessed February 13, 2006).

Cowan, M., and K. Talaro. 2006. Microbiology: A Systems Approach. New York: McGraw-Hill.

Cranmer, H., and M. Martinez. 2007. CBRNE-Anthrax Infection http://www.emedicine.com/emerg/topic864.htm (accessed February 13, 2007).

Cruz, L., E. Fletcher, A. Jones, and N. Prakash. 2004. The history of tuberculosis. http://efletch.myweb.uga.edu/history.htm (accessed May 14, 2005).

Cuthill, S. 2003. Escherichia coli infections. http://www.emedicine.com/ped/ topic2696.htm (accessed October 16, 2005).

Ettinger, S. J., and E. C. Feldman. 2004. Textbook of Veterinary Internal Medicine, 6th ed. Philadelphia, PA: W. B. Saunders.

Factsheets on Chemical and Biological Warfare Agents. 1999. Glanders: essential data. http://www.cbwinfo.com/Biological/ Pathogens/BMa.html (accessed August 22, 2005).

Factsheets on Chemical and Biological Warfare Agents. 1999. Melioidosis: essential data. http://www.cbwinfo.com/Biological/Pathogens/BP.html (accessed August 22, 2005).

Factsheets on Chemical and Biological Warfare Agents. 2005. Brucellosis. http://www.cbwinfo.com/ Biological/Pathogens/BM.shtml (accessed November 11, 2005).

Forbes B., D. Sahm, and A. Weissfeld. 2002. Bailey & Scott's Diagnostic Microbiology, 11th ed. St. Louis, MO: Mosby.

Ghorayeb, Z. N., and M. Matta-Muallem. 2005. Erysipeloid. http://www.emedicine.com/derm/topic602.htm (accessed November 8, 2005).

Harmes, J. 2005. Tuberculosis: death's captain. http://www.bact.wisc.edu (accessed May 15, 2005).

Haubrich, W. S. 1997. Medical Meanings: A Glossary of Word Origins. Washington, DC: American College of Physicians.

Herchline, T. 2005. Staphylococcal infections. http://www.emedicine.com/med/ topic2166.htm (accessed July 6, 2005).

Hnilica, K., and E. May. n.d. Staphylococcus pyoderma: an emerging crisis. http://www.utskinvet.org/pdf/staphylococcus_an_emerging_crisis.pdf (accessed July 20, 2005).

Ingraham, J., and C. Ingraham. 2004. Introduction to Microbiology: A Case History Approach, 3rd ed. Pacific Grove, CA: Thomson Brooks Cole.

Institute for International Cooperation in Animal Biologics, Iowa State University. 2005. Streptococcosis. http://www.cfsph.iastate.edu/Factsheets/pdfs/ streptococcosis.pdf (accessed June 15, 2005).

Jakowski, R., and G. Kaufman. 2004. Avian Bacterial, Mycoplasmal and Chlamydial Diseases. Tufts Open Course Ware. http://www.myoops.org/twocw/tufts/ courses/5/content/215761.htm (accessed November 12, 2005).

Jani, A. 2003. Pseudotuberculosis Yersinia. http://www.emedicine.com/med/ topic1947.htm (accessed July 28, 2003).

Johnstom, W., M. Eidson, K. Smith, and M. Stobierski. 2000. Compendium of measures to control Chlamydia psittaci infection among humans (psittacosis) and pet birds (avian chlamydiosis), 2000. Morbidity and Mortality Weekly Review 49(RR14):1-17.

Joint FAO/WHO Expert Committee on Brucellosis. 1986. Sixth Report, Technical Report Series 740. Geneva: World Health Organization.

Jones, T. C., R. D. Hunt, and N. W. King. 1997. Veterinary Pathology, 6th ed. Baltimore, MD: Williams & Wilkins.

Kaneene, J., and C. Thoen. 2004. Zoonosis update: tuberculosis. Journal of the American Veterinary Medical Association 224(5):685-91.

Kotloff, K. L., et al. 1999. Global burden of Shigella infections: implications for vaccine development and implementation of control strategies. Bull World Health Organ 77(8):651-66.

Krauss, H., A. Weber, M. Appel, B. Enders, H. D. Isnebergy, H. G. Schiefer, W. Slenczka, A. von Graeventiz, and H. Zahner. 2003. Zoonoses Infectious Diseases Transmissible From Animals to Humans, 3rd ed. Washington, DC: ASM Press.

Kumamoto, K. S., D. J. Vukich. 1998. Clinical infections of Vibrio vulnificus: a case report and review of the literature. Journal of Emergency Medicine 16(1):61-66.

Lappin, M. R. 2004. Zoonotic diseases: What you can catch at work Parts I and II. The NAVTA Journal Fall:33-45.

Lundstrom, K., and G. Allen. 2005. Cat Scratch Disease. http://www.emedicine.com/ ent/topic523.htm (accessed April 3, 2005).

Maloney, G., and W. Fraser. 2006. Brucellosis. http://www.emedicine.com/emerg/ topic883.htm (accessed May 10, 2006).

Martin, B. Institutional Animal Care and Use Committee. 1996. Zoonotic diseases. http://research.ucsb.edu (accessed February 23, 2005).

Medline Plus. 2005. Brucellosis. http://www.nlm.nih.gov/medlineplus/ency/article/ 000597.htm (accessed November 11, 2005).

Medline Plus. 2005. E. coli infections. http://www.nlm.nih.gov/medlineplus/ ecoliinfections.html (accessed January 12, 2006).

Medline Plus. 2005. Leprosy. http://www.nlm.nih.gov/medlineplus/ency/article/ 001347.htm (accessed October 30, 2005).

Medline Plus. 2005. Salmonellosis. http://www.nlm.nih.gov/medlineplus/ salmonellainfections.html (accessed September 5, 2005).

Medline Plus. 2005. Tuberculosis. http://www.nlm.nih.gov/medlineplus// tuberculosis.html (accessed May 10, 2005).

Medline Plus. 2006. Gas gangrene. http://www.nlm.nih.gov/medlineplus/ency/ article/000620.htm (accessed February 17, 2006).

Medline Plus. 2006. Rat-bite fever. http://www.nlm.nih.gov/medlineplus/ency/ article/001348.htm (accessed November 27, 2006).

Merck Veterinary Manual. 2006. Clostridia-associated enterocolitis infections. http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/ 22205.htm&word=clostridial%2cinfection (accessed February 13, 2006).

Merck Veterinary Manual. 2006. Staphylococcus: introduction. http:// www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/204200.htm&word= staphylococcal%2cinfection (accessed February 13, 2006).

Merck Veterinary Manual. 2006. Vibriosis. http://www.merckvetmanual.com/mvm/servlet/ CVMHighLight?file=htm/bc/tzns01.htm&word=vibrio (accessed July 26, 2006).

Minnaganti, V., and B. Cunha. 2003. Plague. http://www.emedicine.com/MED/ topic3381.htm (accessed January 22, 2003).

Mylonakis, E., C. Go, and B. Cunha. 2006. Escherichia coli infections. http://www.emedicine.com/med/topic734.htm (accessed May 26, 2006).

National Center for Animal Health Programs. 2006. OIE Listed Diseases. http://www.aphis.usda.gov/vs/ncie/oie/rtf_files/ animal-dis-noti_dec03.rtf (accessed March 1, 2006).

National Tuberculosis Center. 1996. Brief history of tuberculosis. http://www.umdnj.edu/~ntbcweb/history.htm (accessed May 10, 2005).

Netahlo-Barrett, L. n.d. The bubonic plague (Yersinia pestis): The black death. http://militaryhistoryonline.com (accessed April 10, 2005).

Oba, Y., and G. Salzman. 2005. Chlamydial pneumonias. http://www.emedicine.com/ med/topic341.htm (accessed March 8, 2005).

Office of Communications and Public Liaison, Anthrax, National Institutes of Health, United States Department of Health and Human Services. 2002. The Jordan Report 20th Anniversay Accelerated Development of Vaccines, 2002. http://www.niaid.nih.gov/dmid/vaccines/jordan20/jordan20_2002.pdf (accessed May 15, 2002) pp. 3-261.

Olson, C. 2004. Campylobacter. http://www.vetmed.wisc.edu/pbs/zoonoses/ GIk9fel/campylobacter.html (accessed April 14, 2005).

Olson, C. 2004. Streptococcal zoonoses. http://www.vetmed.wisc.edu/pbs/ zoonoses/Streptococcus/strpindex.html (accessed January 4, 2006).

Olson, C. 2004. Zoonosis Tutorial, Tuberculosis. zoonoses http://www.vetmed.wisc.edu/pbs/zoonoses/Streptococcus/ strpindex.html (accessed May 11, 2005).

Olson, C., and G. Mejicano. Partners in Agriculture Health. n.d. Erysipelothrix rhusiopathiae infection. Module VI. http://worh.org/new_orh_docs/ farmershealth/pdf_etc/fhpdf/zoon.pdf (accessed February 23, 2005).

Pelzer, K. D. 1995. Salmonellosis: Zoonosis Updates, 2nd ed. Schaumburg, IL: AVMA.

Perry, D., and J. Fetherston. 1997. Yersinia pestis: etiologic agent of plaque. Clinical Microbiology Reviews 10(1):35-66.

Prescott, L. M., D. A. Klein, and J. P. Harley. 2002. Microbiology, 5th ed. New York: McGraw-Hill.

Rao, P., S. Riccardi, and D. Birrer. 2004. The history of salmonellosis. www. columbia.edu/cu/biology/courses/g4158/presentations/2004/Salmonella.ppt (accessed September 14, 2005).

Reboli, A., and W. E. Farrar. 1989. Erysipelotrhix rhusiopathiae: an occupational pathogen. Clinical Microbiology Reviews 2 (4):354-9.

Rega, P., and D. Batts. 2005. CBRNE: Glanders and Melioidosis. http://www.emedicine.com/emerg/topic884.htm (accessed April 6, 2005).

Regnery, R., and J. Tappero. 1995. Unraveling mysteries associated with cat-scratch disease, bacillary angiomatosis, and related syndromes. Emerging Infectious Diseases 1(1):16-21.

Rollins, D. M., and S. W. Joseph. 2000. Campylobacter. http://www.clfs.umd.edu/classroom/bsci424/PathogenDescriptions/ Campylobacter.htm (accessed May 24, 2005).

Sack, D. A. 1998. Cholera and related illnesses caused by Vibrio species and Aeromonas. In Infectious Diseases, edited by S. L. Gorbach, J. G. Bartlett, and N. R. Blacklow. Philadelphia, PA: W. B. Saunders Co.

Schwartzman, W. A. 2000. Cat scratch disease and other bartonella infections. Current Treatment Options in Infectious Diseases 2:155-62.

Shimeld, L. A. 1999. Essentials of Diagnostic Microbiology. Albany, NY: Delmar Publishers.

Short, B. 2002. Pasteurellosis: an important emerging infectious disease--a military problem? ADF Health 3(1):13-21.

Smith, B. P. 2001. Large Animal Internal Medicine, 3rd ed. St. Louis, MO: Mosby.

Smith, K., K. Bradley, M. Stobierski, and L. Tengelsen. 2005. Compendium of measures to control Chlamydophila psittaci (formerly Chlamydia psittaci) infection among humans (psittacosis) and pet birds. http://www.avma.org/pubhlth/psittacosis.asp (accessed November 12, 2005).

Stump, J. L. 2004. Animal bites. http://www.emedicine.com/emerg/topic60.htm (accessed October 12, 2004).

Subekti, D., B. Oyofo, P. Tjaniadi, A. Corwin, W. Larasati, M. Putri, C. Simanjuntak, N. Punjabi, J. Taslim, B. Setiawan, A. Agung, G. S. Djelantik, L. Sriwati, A. Sumardiati, E. Putra, J. Campbell, and M. Lesmana. 2001. Shigella spp. surveillance in Indonesia: the emergence or reemergence of S. dysenteriae. Emerging Infectious Diseases 7(1):137-40.

Taplitz, R. A. 2004. Managing bite wounds. Postgraduate Medicine Online. http://www.postgradmed.com (accessed June 23, 2005).

Todar, K. 2003. Listeria monocytogenes and Listeriosis. In Todar's Online Textbook of Bacteriology. http://textbookofbacteriology.net/Listeria.html (accessed May 1, 2005).

Todar, K. 2005. Bacillus anthracis and anthrax. In Todar's Online Textbook of Bacteriology. http://textbookofbacteriology.net (accessed April 14, 2005).

Todar, K. 2005. The pathogenic Clostridia. In Todar's Online Textbook of Bacteriology. http://textbookofbacteriology.net/clostridia.html (accessed May 21, 2005).

USDA APHIS. 2005. Brucellosis, National Center for Animal Health Programs. http://www.aphis.usda.gov/vs/nahps/brucellosis/ (accessed July 30, 2005).

Wassenaar, T. 2005. Virtual Museum of Bacteria. http://www.bacteriamuseum.org (accessed April 15, 2005).

Weese, J. 2002. A review of equine zoonotic diseases: risks in veterinary medicine. AAEP Proceedings 48:362-9.

Wong, J., and W. Reenstra-Buras. 2006. Gas gangrene. http://www.emedicine.com/emerg/topic211.htm (accessed January 31, 2006).

World Health Organization. 2000. Cholera. http://www.who.int/mediacentre/ factsheets/fs107/en/ (accessed April 25, 2005).

World Health Organization. 2001. Water-related Diseases: Leptospirosis. http://www.who.int/water_sanitation_health/diseases/leptospirosis/en/ (accessed November 12, 2005).

World Health Organization. 2005. Brucellosis. http://www.who.int/zoonoses/ diseases/brucellosis/en/ (accessed November 11, 2005).

World Health Organization. 2005. Leprosy. http://www.who.int/mediacentre/ factsheets/fs101/en/ (accessed October 30, 2005).

World Health Organization. 2005. Salmonellosis. http://www.who.int/topics/ salmonella/en/ (accessed September 14, 2005).

World Health Organization. 2005. Shigellosis. http://www.who.int/ vaccine_research/diseases/shigella/en/ (accessed September 17, 2005).

World Health Organization. 2005. Tuberculosis. http://www.who.int/mediacentre/ factsheets/fs104/en/index.html (accessed May 10, 2005). World Health Organization. n.d. Water sanitation: Introduction. http://www.who.int/water_sanitation_health/bathing/ recreadischap1.pdf (accessed January 12, 2006).

Young, E. J., and M. J. Corbel, eds. 1989. Brucellosis: Clinical and Laboratory Aspects. Boca Raton, FL: CRC Press.

Zach, T. 2006. Listeria infection. http://www.emedicine.com/PED/topic1319.htm (accessed February 27, 2006).

Zapor, M., and D. Dooley. 2005. Salmonellosis. http://www.emedicine.com/med/ topic2058.htm (accessed August 2, 2005).
Table 3-8 Streptococcus spp. and Their Features

Species                Lancefield Group   Habitat

Str. Pyogenes *        A                  Human throat

Str. agalactiae        B                  Vaginal tract of some women
                                          GI and urinary tracts of
                                          people Udder of cow

Str. dysgalactiae      A, C, G, and L     Swine, dogs, cats, poultry,
subspecies                                and cattle
equisimilis (#)

Str. dysgalactiae      A, C, G, and L     Variety of animals
subspecies
dysgalactiae

Str. equi subspecies   C                  Various mammals
equi                                      (mainly horses)

Str. equi subspecies   C                  Large spectrum of animal
zooepidemicus (#)                         species

Str. Suis (#)          R, S, and T        Swine, ruminants, bison,
                                          humans

Str. Canis (#)         G                  Dogs, cats, humans

Str. Iniae (#)         No Lancefield      Freshwater fish, dolphins,
                       grouping           humans

Str. Porcinus (~)      E, P, U, V,        Swine, humans
                       none, and new

Str. bovis group (~)   D                  Normal flora of humans
                                          and animals

Str. pneumoniae (~)    No Lancefield      Horses, Guinea pigs, rats,
                       grouping           humans

viridans               No Lancefield      Commensal in many
Streptococcus          grouping           animals
group (~)

Species                Disease

Str. Pyogenes *        Strep throat, scarlet fever, impetigo,
                       erysipelas, necrotizing fasciitis,
                       streptococcal toxic shock syndrome

Str. agalactiae        Neonatal septicemia, meningitis, pneumonia,
                       and death in humans; mastitis in cattle

Str. dysgalactiae      Various infections in animals; pharyngitis
subspecies             and endocarditis in humans
equisimilis (#)

Str. dysgalactiae      Skin and respiratory infections (dog and cats),
subspecies             mastitis (cattle), septicemia, arthritis, and
dysgalactiae           meningitis (pigs), and nasopharygeal
                       infections (poultry)

Str. equi subspecies   Strangles in horses
equi

Str. equi subspecies   Wound infections, endometritis, arthritis,
zooepidemicus (#)      and mastitis in animals; bacteremia,
                       meningitis, and streptococcal toxic shock
                       syndrome in humans

Str. Suis (#)          Meningitis, septicemia, and arthritis in pigs;
                       meningitis and hearing loss in humans

Str. Canis (#)         Otitis media, septicemia, lymphadenopathy,
                       polyarthritis, reproductive tract infections,
                       and mastitis in dogs; wound infections and
                       bacteremia in humans

Str. Iniae (#)         Abscesses and skin infections in fish;
                       cellulitis, meningitis, and endocarditis
                       in humans

Str. Porcinus (~)      Isolated from swine and humans, but incidence
                       of infection unknown

Str. bovis group (~)   Endocarditis, urinary tract infections,
                       osteomyelitis, and sepsis in humans

Str. pneumoniae (~)    Respiratory disease in horses, Guinea pigs,
                       and rats; number one cause of bacterial
                       pneumoniae in humans

viridans               May cause endocarditis and other infections
Streptococcus          in humans
group (~)

* Can cause reverse zoonosis in dogs, udders of cows

(#) zoonotic

(~) zoonotic potential uncertain

Table 3-9 Less Common Bacterial Zoonoses

                                             Predominant Signs
Bacterium            Bacterial Description   in People

Actinobacillus       Gram-negative rod       Wounds with abscess
lignieressi,                                 formation are seen on
A. equuli,                                   hands and forearms;
A. suis                                      septicemia may occur

Aeromonas spp.       Gram-negative rod       Diarrhea;
(A. caviae,                                  gastroenteritis,
A. hydrophila,                               skin wounds
A. sobia,                                    Healthy people can
A. jandaei,                                  contract this
A. schubertii,                               bacterium; however,
A. veronii)                                  children are more
                                             prone to this illness
                                             than any other age
                                             group Those with weak
                                             immune systems
                                             develop septicemia

Arcanobacterium      Gram-positive           Septicemia, endo-
pyogenes (formerly   curved rod              carditis, meningitis,
Corynebacterium                              arthritis, pneumonia,
pyogenes and                                 and abscesses on
Actinomyces                                  extremities
pyogenes)

Bordetella           Gram-negative rod       Pertussis-like
bronchiseptica                               disease in
                                             immunecompromised
                                             people

Corynebacterium      Gram-positive rod       Necrotixing
pseudotuberculosis                           lymphadentitis of
                                             mandibular, axillar,
                                             or inguinal lymph
                                             nodes

Corynebacterium      Gram-positive rod       Diphtheria-like sore
ulcerans                                     throat

Dermatophilus        Gram-positive           Eczema-like lesion,
congolensis          branching               pustules, or
                     filaments               furuncles on the
                                             hands and forearms

Edwardsiella         Gram-negative rod       Wide variety of
tarda                                        infections in immune-
                                             compromised people
                                             (usually in normally
                                             sterile sites such as
                                             the lungs, urinary
                                             tract, and blood)

Helicobacter         Gram-negative           Gastric ulcers and
spp.                 spirillum               gastritis
                                             (H. pylori);
                                             enteritis and sepsis
                                             (H. cinaedi and
                                             H. fennelliae); other
                                             species in animals
                                             include
                                             H. canis, H. felis,
                                             and H. suis

Rhodococcus          Gram-positive,          Pulmonary infections
equi                 slightly acid-fast      in immune compro-
                     rod                     mised people

Bacterium            Transmission            Animal Source

Actinobacillus       Animal bites; direct    Normal oropharyngeal
lignieressi,         contact with            bacteria of horses,
A. equuli,           preexisting wounds      cattle, sheep, and
A. suis              during exposure         pigs
                     to animals

Aeromonas spp.       Ingestion of            Fresh aquatic
(A. caviae,          contaminated food or    environments;
A. hydrophila,       water; skin or mucous   various warm- and
A. sobia,            membrane exposure to    cold-blooded
A. jandaei,          contaminated water;     animals
A. schubertii,       skin trauma by fish
A. veronii)          fin or fish hook;
                     seafood

Arcanobacterium      Direct transmission     Normal bacteria of
pyogenes (formerly   from animals to         cattle, sheep, and
Corynebacterium      humans not proven;      pig mucous membranes
pyogenes and         fly vector possible
Actinomyces
pyogenes)

Bordetella           Aerosols or close       Normal bacteria of
bronchiseptica       contact with infected   horses, pigs, dogs,
                     animals                 cats, rabbits, and
                                             Guinea pigs (has
                                             caused respiratory
                                             disease in this
                                             animals as well)

Corynebacterium      Consumption of raw      Normal bacteria of
pseudotuberculosis   milk; close contact     sheep, goats, horses,
                     with infected animals   and cattle (may cause
                                             caseous lymphadenitis
                                             in sheep)

Corynebacterium      Consumption of raw      Normal bacteria of
ulcerans             milk; close contact     cattle (can cause
                     with animals            mastitis in cattle)
                     especially in summer

Dermatophilus        Contact with infected   Source is soil that
congolensis          animals or animal       causes suppurative
                     products; fly vectors   skin disease in wild
                                             and domestic animals
                                             (most frequently
                                             cattle, sheep, and
                                             horses)

Edwardsiella         Uncertain; most         Gastrointestinal
tarda                likely close contact    tract of cold-blooded
                     with contaminated       animals (reptiles)
                     water or infected
                     animal

Helicobacter         Unknown other than      Humans and hamsters
spp.                 that the bacterium is   (H. pylori); other
                     obtained orally         species have been
                                             found in pigs,
                                             cattle, dogs, and
                                             cats

Rhodococcus          Contact with infected   Source is soil that
equi                 animals may be source;  causes pneumonia
                     most common route       in foals and sporadic
                     is through              infections in cattle,
                     contaminated soil       sheep, and pigs

                     Geographic
Bacterium            Distribution            Diagnosis

Actinobacillus       Worldwide               Bacterial culture on
lignieressi,                                 blood agar and
A. equuli,                                   biochemical tests
A. suis

Aeromonas spp.       Worldwide               Bacterial culture on
(A. caviae,                                  blood and MacConkey
A. hydrophila,                               agars and biochemi-
A. sobia,                                    cal tests (string
A. jandaei,                                  test differentiates
A. schubertii,                               it from Vibrio spp.)
A. veronii)

Arcanobacterium      Worldwide               Bacterial culture on
pyogenes (formerly                           blood, chocolate,
Corynebacterium                              Columbia colistin-
pyogenes and                                 nalidixic acid (CNA)
Actinomyces                                  agar and biochemical
pyogenes)                                    tests

Bordetella           Worldwide               Bacterial culture on
bronchiseptica                               blood and MacConkey
                                             agar and biochemical
                                             tests

Corynebacterium      Worldwide; more         Bacterial culture on
pseudotuberculosis   frequent in Australia   blood and commercial
                     and New Zealand         identification (API)
                                             agars and biochemical
                                             tests (identification
                                             is complex in this
                                             genus of bacteria)

Corynebacterium      United Kingdom          Bacterial culture on
ulcerans                                     blood and commercial
                                             identification (API)
                                             agars and biochemical
                                             tests (identification
                                             is complex in this
                                             genus of bacteria)

Dermatophilus        Worldwide, but more     Gram stain, bacterial
congolensis          prevalent in humid,     culture on routine
                     tropical, and           agars such as blood
                     subtropical regions     and Sabouraud
                     such as Africa,         dextrose, and
                     Australia,              biochemical tests
                     New Zealand,
                     and India

Edwardsiella         Worldwide               Gram stain,
tarda                                        bacterial culture on
                                             blood, MacConkey,
                                             and HE or XLD agar,
                                             and biochemical tests

Helicobacter         Worldwide               Stained tissue biopsy
spp.                                         and bacterial culture
                                             on selective agar
                                             such as Skirrow's and
                                             modified
                                             Thayer-Martin
                                             agar may require
                                             1 week; serology for
                                             H. pylori

Rhodococcus          Worldwide               Gram and acid-fast
equi                                         stain, culture on
                                             routine agars such
                                             as blood and
                                             Sabouraud dextrose,
                                             and biochemical tests

Bacterium            Treatment

Actinobacillus       B-lactam antibiotics
lignieressi,         or fluoroquinolones
A. equuli,
A. suis

Aeromonas spp.       Diarrhea may be
(A. caviae,          self-limiting;
A. hydrophila,       cephalosporins,
A. sobia,            quinolones, and
A. jandaei,          aminoglycoside
A. schubertii,       antibiotics
A. veronii)

Arcanobacterium      Usually susceptible to
pyogenes (formerly   penicillin, erythromycin,
Corynebacterium      and clindamycin
pyogenes and
Actinomyces
pyogenes)

Bordetella           Aminoglycoside and
bronchiseptica       quinolone antibiotics;
                     commonly resistant
                     to ampicillin and
                     cephalosporins

Corynebacterium      Vancomycin;
pseudotuberculosis   resistance
                     to penicillins and
                     cephalosporins has
                     been seen

Corynebacterium      Vancomycin; resistance
ulcerans             to penicillins and
                     cephalosporins has
                     been seen

Dermatophilus        Topical antibiotic
congolensis          treatment is usually
                     sufficient

Edwardsiella         Susceptible to many
tarda                antibiotics

Helicobacter         Resistance to antibiotics
spp.                 is a problem; quinolones
                     recommended

Rhodococcus          Antibotic combinations
equi                 such as erythromycin and
                     rifampin
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Title Annotation:Part 5: STREPTOCOCCAL INFECTIONS-References
Author:Romich, Janet Amundson
Publication:Understanding Zoonotic Diseases
Article Type:Disease/Disorder overview
Geographic Code:1USA
Date:Jan 1, 2008
Words:17428
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