Treponemes are strict parasites with complex growth requirements, must cultivate them in live cells.
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1 Chapter 21 Miscellaneous Bacterial Agents of Disease* *Lecture notes are to be used as a study guide only and do not represent the comprehensive information you will need to know for the exams The Spirochetes [I. Spirochetes] Spirochetes are helical, flexible cells with periplasmic flagella (fig. 21.1). Gram negative, the majority of spirochetes are free-living saprobes or commensals of animals and are not primary pathogens. The two most significant exceptions include species belonging to the genera Treponema and Borrelia. See System s Profile 21.1 Miscellaneous Bacterial Pathogens Treponemes: Members of the Genus Treponema [1. Syphilis] Treponemes are strict parasites with complex growth requirements, must cultivate them in live cells. Syphilis, caused by Treponema pallidum pallidum, is a sexually transmitted disease responsible for venereal and congenital syphilis. Treponema pallidum is a motile spirochete (fig. 21.1a & fig. 21.1b). Motility is the result of periplasmic flagella. Obligate anaerobes with a generation time of 4-18 hours. Pathogenic treponemes cannot be cultivated in vitro. See Pathogen Profile #1 Treponema pallidum (T. pallidum pallidum) Treponema pallidum: The Spirochete of Syphilis The exact origin of syphilis is not clear. What is certain is that it is sexually transmitted and can be found worldwide. Epidemiology and Virulence Factors of Syphilis Humans are the natural host and source of T. pallidum. It is fastidious and can not survive outside the host for very long. Syphilis cases were in decline until the 1990 s, but now there is an increase in the number of cases (See fig ). Pathogenesis and Host Response T. pallidum binds to epithelial cells by its hooked tip. The ID = cells. Its outer membrane proteins are part of its infectious process. CLINICAL MANIFESTATIONS Untreated syphilis is marked by clinical stages as primary, secondary, and tertiary. There are multiple signs and symptoms for each stage. Based on these broad descriptions of the signs and symptoms, syphilis can imitate many other diseases. See Table Syphilis is mostly transmitted during the primary and secondary stages. Primary Syphilis Characterized by an ulcerative lesion (chancre) at the site of infection (fig. 21.2). Infection of other individuals can occur. Lymph nodes in the region of organ / tissue infection become enlarged. The chancre will heal, but the person is still highly infectious. Secondary Syphilis After ~ 6 weeks, the chancre heals and the secondary stage appears. The organism has now invaded many tissues and organs of the body. This stage is characterized by a red brown rash all over the skin (fig. 21.3). These skin lesions contain viable spirochetes. 1
2 Latency and Tertiary Syphilis Latency can last for 20 years or longer. The final stage, tertiary syphilis, is rare due to use of antibiotics. There can be multiple organ failure at this stage you see ulcers known as gummas (fig. 21.4). Syphilis is divided into 3 stages (Table 21.1), with different signs and symptoms: 1. primary syphilis = chancre at site of infection, first appearing 3 weeks after infection (fig. 21.2). The lesion is accompanied by lymph node enlargement in the region. The chancre heals in 5-10 days on its own. HOWEVER, if untreated secondary syphilis occurs weeks or months after primary syphilis. Characterized by multiple skin lesions, rashes (fig. 21.3), fever, sore throat, malaise and lymphadenopathy (swelling of the lymph nodes). Lesions can also occur on internal organs at this stage. The lesions contain treponemes and are highly infectious. Antigen-antibody complexes are detectable. If these lodge in kidney glomeruli, kidney damage can result. If they lodge in joints, they can cause arthralgias (pain or gout of the joint). 3. If it is still untreated, years later, tertiary syphilis occurs. Gumma formation, with few if any treponemes (fig. 21.4). Gummas are swollen syphilitic tumors. Cardiovascular diseases, often fatal, occur at this stage when lesions affect aortic valves or cause aortic aneurysms. Final effects include blindness and dementia (insanity). Congenital Syphilis In pregnant women, T. pallidum can cross the placenta and infect the fetus at anytime during the pregnancy where it can multiply in fetal tissue causing congenital syphilis (fig. 21.5). Most commonly, it occurs during the second and third trimesters. The pathogen inhibits fetal development with the possible consequence of spontaneous miscarriage or stillbirth. Infants born with T. pallidum infections have symptoms including nasal discharge, skin eruptions and loss, bone deformation, and nervous system abnormalities. Clinical and Laboratory Diagnosis The stages of syphilis can mimic other diseases. Complications of diagnosing syphilis include the signs and symptoms of each stage can seem unrelated, the chancre and skin rash can imply other bacterial, fungal or parasitic infections. And there can be other STDs such as gonorrhea and chlamydiosis that complicate diagnosis. Special stains using silver can be used to view the cells in bright-field microscopy (fig. 21.6). Patient samples can be tested with DNA probes to determine the presence of the organism. Testing Blood for Syphilis Several antibody tests can be done: RPR, VDRL, and fluorescent antibody tests. Treatment: Penicillin G (So far, there is no penicillin resistance.) Those individuals at most risk should receive regular monitoring. Nonsyphilitic Treponematoses These diseases resemble syphilis, but they are rarely sexually and congenitally transmitted. Bejel Known as nonvenereal childhood syphilis caused by the subspecies T. pallidum endemicum. Seen in people native to Middle East and North Africa. Can be transmitted by direct contact and fomites, enters through breaks in the skin and mucous membranes. The infection starts in the mouth, then moves to the skin and palms (fig. 21.7a). Yaws endemic to warm, humid tropical regions of Africa, Asia, and South America. It caused by the subspecies T. pallidum pertenue. It is spread by direct contact and fomites. Unsanitary and crowded living conditions contribute to the spread. The organism forms a mother yaw on the legs (fig. 21.7b). Pinta is a chronic skin infection caused by T. pallidum carateum. Transmission is by several years of close contact, with poor hygiene. Mostly found in isolated regions of Latin America. Borrelia: Arthropod-Borne Spirochetes [2. Lyme disease] 2
3 Borrelia are morphologically distinct from other spirochetes, they tend to be larger. The bacterium has very specific growth requirements. The Borrelia are transmitted by insect vectors lice and ticks. Borrelia burgdorferi and Lyme Disease Lyme disease was recognized in the United States in An outbreak of arthritis occurred near Lyme, Connecticut. Since then, the disease has increased dramatically. There were over 13,000 cases reported in 1994; by the number of cases had increased to more than 21,000. The greatest concentration of the disease is in areas where there are high mouse and deer populations. See 21.1 MAKING CONNECTIONS Lyme disease is caused by Borrelia burgdorferi, a spirochete (fig. 21.9). The disease is zoonotic 1 : it is transmitted by ticks of the genus Ixodes (figure 21.9b). As a larva or nymph of Ixodes feeds on a mouse (i.e., white-footed mouse in the northeastern U.S., and the dusky-footed wood rat in California), where it picks up Borrelia. The nymph is relatively nonspecific and will feed on any type of warm blooded vertebrate, including humans and their pet dogs and cats. The disease is characterized by a bull's eye lesion (fig 21.9c) at the bite location, fever, headache, achy muscles, stiff neck and dizziness. If untreated or treated too late, the disease can progress causing cardiac dysrhythmias and neurological symptoms such as facial palsy. After several weeks or months, a crippling arthritis can attack the joints. Some people develop chronic neurological complications that are severely disabling. Lyme disease acquired during pregnancy may lead to infection of the fetus and possibly stillbirth. Treatment: Early treatment with tetracycline and amoxicillin has been effective Curviform Gram-Negative Bacteria and Enteric Diseases Vibrio cholerae comma-shaped rods with one flagellum; Campylobacter jejuni short spirals or curved rods with one flagellum; and Helicobacter pylori tight spirals and curved rods with several polar flagella. One common feature to all of these is that they are able to survive the harsh intestinal environment. The Biology of Vibrio cholera [1. Vibrio] Cholera is an acute infection by Vibrio cholerae. Vibrio cholerae is G-, motile by polar flagella, curved or comma-shaped rod (fig ). Oxidase positive, facultative anaerobe. Epidemiology of Cholera El tor biotype is most prevalent worldwide. It can survive longer outside the host. The most recent outbreak was after the 2010 earthquake in Haiti. It ranks at the top in morbidity and mortality world wide, but tends to be rare in the US. If an outbreak does occur, then it is usually near the Gulf of Mexico. The organism enters the human host through contaminated food or water. Infected individuals shed the pathogen into sewage, which contaminates water supplies. Spread of the disease is by the fecal-oral route. Carriers harbor the organism in their gall bladders, just as Typhoid Mary did with typhoid. Pathogenesis of Cholera: Toxigenic Diarrhea 1 Zoonotic (or Zoonosis): infections communicated from animals to humans. 3
4 It is characterized by profuse, watery discharge. Initially diarrhea is brown and then develops to a pale whitish color known as "rice water" because it contains flecks of mucous. It may be accompanied by vomiting. The cells adhere to the microvilli of epithelial cells where they multiply and produce a toxin called cholera toxin (CT). The toxin induces excessive fluid loss from the intestinal cells, up to 1 Liter/hour in extreme cases (fig ). The tremendous fluid loss and loss of electrolytes decreases blood volume and can lead to hypovolemic shock (i.e., shock from loss of blood volume). Hypotension, tachycardia, cyanosis and collapse from shock occurs within hours. If the disease goes untreated, death is in less than 48 hours. There is approximately 55% mortality rate. Diagnosis and Remedial Measures A vaccine does exist for frequent travelers. Treatment: Fluid and electrolyte replacement. Read: 21.2 MAKING CONNECTIONS. Tetracycline reduces the numbers of organisms in the intestine and helps eliminate carrier situation. Vibrio parahaemolyticus and Vibrio vulnificus: Pathogens Carried by Seafood [Vibrio species and seafood] Vibrio parahaemolyticus and V. vulnificus are salt-tolerant species that are often the leading cause of food-poisoning associated with eating raw or undercooked seafood (especially raw oysters). Both cause severe gastroenteritis. Incubation period of about 24 hours followed by profuse watery diarrhea, nausea, vomiting, and abdominal cramps. Treatment requires fluid and electrolyte replacement. Features of V. parahaemolyticus Gastroenteritis V. parahaemolyticus causes an acute gastroenteritis as a result of eating raw, undercooked, or poorly stored seafood. Incubation period is ~24 hours, followed by explosive diarrhea, vomiting, abdominal cramps and fever. This bacterium can produce toxins that cause symptoms for up to 72 hours and persist for 10 days. V. vulnificus symptoms are similar to V. parahaemolyticus. V. vulnificus is most often associated with raw oysters. Prevention of contamination with these organisms includes refrigeration and cooking the seafood at the right temperature. NOTE: Some species of Vibro are capable of causing a necrotizing fasciitis like S. pyogenes (see Ch. 18). These bacteria will infect small cuts and abrasions while a person is swimming in brackish water (for instance Galveston Bay). The symptoms and signs are identical and the condition will spread very quickly. Immediate medical attention is necessary. Diseases of the Campylobacter Vibrios [2. Campylobacter jejuni] C. jejuni is Gram negative, monotrichous flagella, curved rod, microaerophilic and grows best at 40-42ºC (fig ). C. jejuni adhere to the mucosa of the small intestine where they burrow and multiply. Campylobacter jejuni Enteritis Campylobacter jejuni is now considered one of the most important causes of bacterial gastroenteritis worldwide. Primary pathogen transmitted through contaminated beverages and food, especially water, milk, meat, and especially chicken. According to some estimates, approximately 80% of chicken bought in U.S. grocery stores is contaminated with either C. jejuni or Salmonella. 4
5 C. jejuni produces an enterotoxin called CJT. Signs and symptoms develop after 1 to 7 days post-ingestion: Fever and malaise followed by diarrhea (may be bloody) and severe cramping. Lasts less than 1 week and is self-limiting. Electrolyte and fluid replacement necessary. See also Pathogen Profile #2: Campylobacter jejuni Helicobacter pylori: Gastric Pathogen [3. Helicobacter pylori] Although it was first isolated in 1979 and implicated in causing gastritis, Helicobacter pylori has been accepted in recent years as an etiologic agent of stomach ulcers. Ulcer formation is linked to other factors including overproduction of stomach acid (genetic cause or stress). However, H. pylori is now recognized as a very strong contributing factor. Occurring in ~25% of the adult population (60% of people 60 and over), H. pylori seems to be acquired early in life and carried asymptomatically until its activities begin to damage the digestive mucosa. (Fig ) Treatment: Newest recommended therapy for stomach ulcers is 2-4 weeks of clarithromycin to eliminate the bacteria and Zantac to inhibit the formation of stomach acid. An enterotoxin is any toxin produced by a pathogenic organism which acts on the large or small intestine. Note: Typhoid fever is so named only because the symptoms resemble typhus. Typhus is a Rickettsia disease (see chapter 21). The most famous was Mary Mallon - "Typhoid Mary" - who worked as a cook in the early 1900s and spread the infection to hundreds of people before she was forced into a quarantine facility. It is estimated that one out of every three chickens is contaminated with Salmonella. The Komodo dragon s bacteria count is so high that people visiting a zoo who touched the rail of a dragon s cage contracted Salmonella! Do not confuse bacterial dysentery with amebic dysentery, which is caused by the protozoan Entamoeba histolytica and Giardia lamblia. NOTE: This is a zoonotic infection, i.e. an infection acquired from another animal. The rat flea would be considered a biological vector (Ch. 13). Boubon is Greek for groin Vibrio, Campylobacter, and H. pylori are covered in the book s chapter 21; but presented here with the other gram-negative bacilli Medically Important Bacteria of Unique Morphology and Biology [II. Rickettsia] Order Rickettsiales The Order Rickettsiales are obligate to their host cells and require live cells for cultivation. They spend part of their lifecycle in arthropods, which serve as vectors. Rickettsioses are considered emerging diseases. Morphological and Physiological Distinctions of Rickettsias Rickettsias are gram-negative, non-motile pleomorphic rods or coccobacilli which are very small ( μm wide and μm long) (fig ). They are obligate intracellular parasites and require live cells for cultivation. Distribution and Ecology of Rickettsial Diseases The Role of Arthropod Vectors As with Borrelia, the Rickettsia life cycle depends on a complex exchange between blood-sucking arthropods and vertebrate hosts, i.e. these are zoonotic infections. 5
6 General Factors in Rickettsial Pathology and Isolation Rickettsial infections are targeted to the endothelial lining of small blood vessels. The bacteria causes necrosis of the vascular lining. Specific isolation and cultivation of the bacteria from a host is necessary. Specific Rickettsioses Rickettsias are differentiated based on their clinical features and epidemiology (Table 21.2). The two main groups are: (1) the typhus group (2) the spotted fever group Rickettsia prowazekii and Epidemic Typhus (1) A. Epidemic typhus 2 caused by Rickettsia prowazekii; carried by human body lice. Epidemiology of Epidemic Typhus Humans are the sole host of human body lice and the only reservoirs R. prowazekii. Associated with overcrowding and poor sanitation. Disease Manifestations and Immune Response in Typhus Characterized by high fever, chills, headache, and generalized rash. Condition can worsen to include oliguria (low urine output), hypotension, and gangrene secondary infections in areas of poor blood circulation. Potentially fatal, with mortality rates between 40-60% in patients over 50 years of age. The organism can evade the immune system and enter into latency. Treatment and Prevention of Typhus Doxycycline or chloramphenicol are administered. The bacterium can be eradicated by exterminating the vector. Antilouse shampoo or ointment is also effective. Epidemiology and Clinical Features of Endemic Typhus B. Endemic (murine) typhus caused by Rickettsia typhi harbored by mice and rats; their fleas. Symptoms like epidemic form, but milder. Treatment: Tetracycline or chloramphenicol. Rocky Mountain Spotted Fever: Epidemiology and Pathology (2) Rocky Mountain spotted fever (RMSF) caused by R. rickettsi carried by dog and wood ticks; most cases on eastern seaboard (Fig ). Pathogenesis and Clinical Manifestations of Spotted Fever Infection causes distinct spotted, migratory rash; acute reactions include heart and CNS damage (Fig ). 2 Remember: Do not confuse typhus with typhoid fever, an unrelated illness caused by Salmonella typhi. 6
7 Diagnosis, Treatment, and Prevention of Spotted Fever RMSF is potentially fatal and requires immediate treatment with tetracycline (or chloramphenicol) if suspected infection has occurred. Prevent the spread by wearing protective clothing, using insect sprays, and quickly removing ticks. See Pathogen Profile #3 Rickettsia rickettsii Other Obligate Parasitic Bacteria: The Chlamydiaceae [III. Chlamydias] Members of the family Chlamydiaceae are small, obligate intracellular parasites, gram-negative, and have pleomorphic morphology. Primary reservoir is the human body. See Pathogen Profile #4 Chlamydia trachomatis The Biology of Chlamydia and Related Forms Life cycle alternates between two stages and is dependent on host cell phagosomes (fig ). Diseases of Chlamydia trachomatis Two primary strains are the trachoma and lymphogranuloma venereum (LGV) strains. The former attacks squamous or columnar cells of mucous membranes in the eyes, genitourinary tract, and lungs; the latter invades the lymphatic tissue of the genitalia (fig ; fig ). Chlamydial Diseases of the Eye Ocular trachoma (fig a) is an ancient disease which can cause blindness if untreated. Early treatment with tetracycline is highly effective. Infantile conjunctivitis develops when the infant passes through the birth canal of an infected mother (fig b). Sexually Transmitted Chlamydial Diseases C. trachomatis is the etiologic agent of sexually transmitted chlamydiosis the most prevalent bacterial STD in the United States. According to the CDC: In 2007, 1,025,208 Chlamydia infections were reported. Underreporting is substantial because many people are carriers although they are unaware of their infection. Approximately 70% of infected women harbor the bacteria asymptomatically, while 10% of males show no signs or symptoms. An estimated 2.8 million Americans are infected with Chlamydia each year. Reports from Europe indicate that the more severe LGV strain is showing an increase incidence. Causes nongonococcal urethritis in males and cervicitis, endometritis, and salpingitis (pelvic inflammatory disease, PID) in females. Treatment: Urogenital Chlamydia infections are most effectively treated with drugs that act intracellularly, such as tetracyclines (e.g. doxycycline) and azithromycin Mollicutes and Other Cell-Wall-Deficient Bacteria These organisms are called mycoplasmas, they are the smallest self-replicating microbes. They tens to lack a cell wall. Disease of the respiratory tract is associated with Mycoplasma pneumoniae; UTIs are associated with M. hominis and Ureaplasma urealyticum. Biological Characteristics of the Mycoplasmas Without a cell wall, they have no defined shaped, they are pleomorphic. They are not strict parasites, but they are fastidious. They also acquire certain lipids from their host cell membrane (fig b). Infections are chronic and difficult to eliminate as the bacterium can bind to receptor proteins on the host cell. 7
8 Mycoplasma pneumonia and Atypical Pneumonia M. pneumoniae is the causative agent of primary atypical pneumonia (PAP). It is easily passed by droplets in close living conditions. Community resistance is high, fatalities are rare. Also known as walking pneumonia. Diagnosis The bacterium can take up to 3 weeks to culture, so diagnosis relies on ruling out other causes of pneumonia. Serological tests are useful in diagnosis. Treatment is done by doxycycline and azrithromycin. It is important to control contamination of this organism on fomites. Other Mycoplasmas M. genitalium and Ureaplasma urealyticum are found in the reproductive tract of newborns and adults. U. ureaplasma has been implicated in nongonococcal urethritis and prostatitis. It has also been linked to miscarriage, still birth and premature births. M. genitalium is an STD. It is common in the genital tract of men and women. In women it can cause cervicitis and vaginitis. In men it can cause NGU and epididymitis. Bacteria That Have Lost Their Cell Walls Exposure of bacteria to drugs like penicillin and enzymes like lysozyme can cause them to lose their cell wall, thus they are called L forms of bacteria. They are not related to mycoplasmas. L forms and Disease Antimicrobic therapy can induce certain bacteria to convert to L forms. It is hard to treat these bacteria with antibiotics that target the cell wall. Some infectious agents that may convert to the L form are group A strep., Proteus, and Corynebacterium. Some people with Crohn s disease have been linked to L forms of bacteria. 8
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