Coxiella burnetii, S.aureus and Mycobacterium in the GI tract By :Nader Alaridah MD, PhD
Coxiella burnetii Coxiella burnetii is a small obligate intracellular organism that has a membrane similar to gram-negative bacteria. C burnetii, causes Q fever. Because it is easily dispersed as an aerosol, C. burnetii is a potential agent of bioterrorism. This organism may survive pasteurization at 60 C for 30 minutes and can survive for months in dried feces or milk. This may be because of the formation of endospore-like structures by C burnetii which make it also is resistant to drying. Coxiella can cause endocarditis (with a rise in the titer of antibodies to C burnetii, phase 1 ) in addition to pneumonitis and hepatitis. Coxiellae grow only in cytoplasmic vacuoles.
Antigens and Antigenic Variation When grown in cell culture, C burnetii exhibits various phases. These phases are associated with differences in virulence. Phase I is the virulent form that is found in humans with Q fever and infected vertebrate animals. It is the infectious form of the organism and the lipopolysaccharide expressed during this phase appears to be a key virulence factor. Phase II forms are not infectious and occur only by serial passage in cell cultures. Patients with clinical illness mount antibodies to both phase I and phase II antigens. It has been proposed that endospores formed by C burnetii contribute to its persistence and dissemination.
Epidemiology C burnetii is found in ticks, which transmit the agent to sheep, goats, and cattle, but transmission by ticks to humans is uncommon. Workers in slaughterhouses and in plants that process wool and cattle hides have contracted the disease as a result of handling infected animal tissues. C burnetii is transmitted by the respiratory pathway rather than through the skin. There may be a chronic infection of the udder of the cow or goat. In such cases, the rickettsiae are excreted in the milk and rarely may be transmitted to humans by ingestion of unpasteurized milk.
Clinical finding : Q FEVER Q fever is a zoonosis. Q fever encompasses two broad clinical syndromes: acute and chronic infection. The host s immune response (rather than the particular strain) most likely determines whether chronic Q fever develops. The symptoms of acute Q fever are nonspecific; common among them are fever, extreme fatigue, photophobia, and severe headache that is frequently retro-orbital. Other symptoms include chills, sweats, nausea, vomiting, and diarrhea, each occurring in 5 20% of cases. After the usual incubation period of 3 30 days, patients with acute Q fever may present with hepatitis (40%), both pneumonia and hepatitis (20%), pneumonia (17%), isolated fever (14%), CNS involvement (2%), and pericarditis or myocarditis (1%). Chronic Q fever is infection that lasts more than 6 months. Infective endocarditis is the most common form of disease in this phase. C. burnetii survives in monocytes from patients with chronic Q fever but not in monocytes from patients with acute Q fever or from uninfected subjects
Diagnosis The diagnosis of Q fever relies on a high index of suspicion as suggested by the epidemiologic features and is proven by serologic analysis. The organism is very infectious, and isolation ought to be done in biosafety level 3 laboratories. Most cases of Q fever are diagnosed based on detection of phase I and II antibodies (between acute and convalescent paired sera); a 4-fold rise in complement-fixing antibody titer against phase II antigen occurs and yields the highest specificity. The 3 serologic techniques used for diagnosis include indirect immunofluorescence (IIF) (method of choice), complement fixation, and enzymelinked immunosorbent assay (ELISA) (comparable to IIF).
Treatment Doxycycline is the drug of choice for the treatment of acute Q fever. The newer macrolides have also been shown to be effective in the treatment of acute pneumonia. Chronic Q fever requires prolonged treatment for 18 months or longer with a combination of doxycycline and hydroxychloroquine. Duration of treatment is long as mentioned earlier and should be determined by decrease in phase I antibody titers. In endocarditis, combination therapy is necessary to prevent relapse; occasionally, valve replacement is required and can prolong survival.
Prevention Good animal-husbandry practices are important in preventing widespread contamination of the environment by C. burnetii. Vaccination of sheep and goats and a culling programs are effective. The presently recommended conditions of high-temperature, short-time pasteurization at 71.5 C for 15 seconds are adequate to destroy viable Coxiella species. For C burnetii, an investigational vaccine made from infected egg yolk sacs is available. This vaccine has been used for laboratory workers who handle live C burnetii but currently is only commercially available in Australia.
Staphylococcus aureus Staphylococcus aureus, the most virulent of the many staphylococcal species, has demonstrated its versatility by remaining a major cause of morbidity and mortality worldwide despite the availability of numerous effective anti-staphylococcal antibiotics. S. aureus is a pluripotent pathogen, causing disease through both toxin- and nontoxin-mediated mechanisms. S. aureus is both a commensal and an opportunistic pathogen. Approximately 30% of healthy persons are colonized with S. aureus, with a smaller percentage (~10%) persistently colonized Staphylococci, gram-positive cocci in the family Micrococcaceae, form grapelike clusters on Gram s stain S. aureus are catalase-positive (unlike streptococcal species), non-motile, aerobic, and facultatively anaerobic.
Pathogenesis S. aureus is a pyogenic pathogen known for its capacity to induce abscess formation at sites of both local and metastatic infections. This classic pathologic response to S. aureus defines the framework within which the infection will progress. The bacteria elicit an inflammatory response characterized by an initial intense infiltration of PMNs and a subsequent infiltration of macrophages and fibroblasts. Either the host cellular response (including the deposition of fibrin and collagen) contains the infection, or infection spreads to the adjoining tissue or the bloodstream. In toxin-mediated staphylococcal disease, infection is not invariably present. For example, once toxin has been elaborated into food, staphylococcal food poisoning can develop in the absence of viable bacteria. In staphylococcal toxic shock syndrome (TSS), conditions allowing toxin elaboration at colonization sites (e.g., the presence of a superabsorbent tampon) suffice for initiation of clinical illness.
Staphylococcal food poisoning S. aureus is among the most common causes of foodborne outbreaks of infection. Staphylococcal food poisoning results from the inoculation of toxin-producing S. aureus into food by colonized food handlers. Toxin is then elaborated in such growth-promoting food as custards, potato, salad, or processed meats. Even if the bacteria are killed by warming, the heat-stable toxin is not destroyed. The onset of illness is rapid, occurring within 1 6 h of ingestion. The illness is characterized by nausea and vomiting, although diarrhea, hypotension, and dehydration may also occur. The differential diagnosis includes diarrhea of other etiologies, especially that caused by similar toxins (e.g., the toxins elaborated by Bacillus cereus). The rapidity of onset, the absence of fever, and the epidemic nature of the presentation (without second-degree spread) arouse suspicion of staphylococcal food poisoning. Symptoms generally resolve within 8 10 h. The diagnosis can be established by the demonstration of bacteria or the documentation of enterotoxin in the implicated food. Treatment is entirely supportive.
Diagnosis If the history and the stool examination indicate a noninflammatory etiology of diarrhea and there is evidence of a common-source outbreak, questions concerning the ingestion of specific foods and the time of onset of the diarrhea after a meal can provide clues to the bacterial cause of the illness.
Treatment The mainstay of treatment is adequate rehydration. Therapy for staphylococcal food poisoning is entirely supportive.
Prevention Wash hands and under fingernails thoroughly with soap and water before handling and preparing food. Do not prepare food if you are ill. If you have wounds or infections on your hands or wrists, wear gloves while preparing food. Keep kitchens and food serving areas clean. If food is to be stored longer than two hours, keep hot foods hot (warmer than 140 F) and cold foods cold (40 F or colder). Store cooked food in a wide, shallow container and refrigerate as soon as possible.
Mycobacterium Tuberculosis (Mtb) It was not until the 19th century, when Robert Koch utilized s new staining method (ZN stain) and applied it to sputum from patients discovering the causal agent of the disease Tuberculosis (TB); Mtb or Koch bacillus. Tuberculosis, consumption(consume patients,weight loss), white plaque (extreme pallor seen among patients) The family mycobacterium tuberculosis complex(mtc) can cause Tuberculosis (TB) in humans and other livings. It includes M. tuberculosis (Mtb), Mycobacterium africanum, Mycobacterium bovis, Mycobacterium microti, Mycobacterium caprae, Mycobacterium pinnipedii, Mycobacterium suricatte, Mycobacterium mungi, Mycobacterium dassie, Mycobacterium oryx and Mycobacterium canetti. Mtb is a slow growing,obligate aerobe, facultative intra- cellular bacterium. Non-spore forming, non-motile acid fast bacilli.
Mycobacterium Tuberculosis (Mtb) staining
TB is considered an airborne infectious disease although M. tuberculosis complex organisms can be spread through un-pasteurised milk, direct inoculation and other means. Epidemiology Two TB-related conditions exist; latent TB infection (LTBI) and TB disease. If not treated properly, TB disease can be fatal. People who have latent TB infection do not feel sick, do not have any symptoms, and cannot spread TB to others About one third of the worlds population is infected with TB bacteria (TB latency). However, only small proportion of those infected will become sick with TB. TB remains a leading cause of infectious diseases morbidity and mortality. In 2015, an estimated 10.4 million new TB cases were seen world wide.
Tuberculosis TB The primary site of TB is usually lung, from which it can get disseminated into other parts of the body. The other routes of spread can be contiguous involvement from adjacent tuberculous lymphadenopathy or primary involvement of extrapulmonary organ. TB bacteria can attack any part of the body such as the pleura,l.n.,pericardium, kidney, spine, brain and abdomen ( abdominal Tuberculosis) collectively known as extrapulmonary TB. The abdominal TB, which is not so commonly seen as pulmonary TB, can be a source of significant morbidity and mortality and is usually diagnosed late due to its nonspecific clinical presentation. The abdominal TB usually occurs in four forms: tuberculous lymphadenopathy, peritoneal tuberculosis, gastrointestinal (GI) tuberculosis and visceral tuberculosis involving the solid organs
Gastrointestinal (GI) tuberculosis pathogenesis Abdominal tuberculosis (TB) includes involvement of the gastrointestinal tract, peritoneum, lymph nodes, and/or solid organs.abdominal TB comprises around 5 percent of all cases of TB Tuberculosis of the abdomen may occur via reactivation of latent TB infection or by ingestion of tuberculous mycobacteria (as with ingestion of unpasteurized milk, or sputum or undercooked meat). In the setting of active pulmonary TB or miliary TB, abdominal involvement may develop via hematogenous spread via contiguous spread of TB from adjacent organs (such as retrograde spread from the fallopian tubes) or via spread through lymphatic channels The mucosal layer of the GI tract can be infected with the bacilli with formation of epithelioid tubercles in the lymphoid tissue of the submucosa. After 2-4 wk, caseous necrosis of the tubercles leads to ulceration of the overlying mucosa which can later spread into the deeper layers and into the adjacent lymph nodes and into peritoneum. Rarely, these bacilli can enter into the portal circulation or into hepatic artery to involve solid organs like liver, pancreas and spleen
Gastrointestinal TB clinical finding The clinical presentation tends to be non-specific, with abdominal pains and general complaints. Although any portion of the gastrointestinal tract may be affected, the terminal ileum and the cecum are the sites most commonly involved. Abdominal pain (at times similar to that associated with appendicitis) and swelling, obstruction, hematochezia, and a palpable mass in the abdomen are common findings at presentation. Fever, weight loss, anorexia, and night sweats are also common.
Laboratory diagnostic methods Smear microscopy Three specimens from each patient with suspected TB should be examined microscopically for Acid Fast Bacilli AFB (classically Ziehl-Neelsen) or mycobacteria can be demonstrated by yellow fluorescence after staining with auramin. Culture Both liquid and solid mycobacterial cultures should be performed for every specimen, and recovered isolates should be Caccording to standard criteria (Lowenstein-Jensen or Middlebrook 7H10), Radiometric broth culture (BACTEC radiometric system). mycobacterial growth indicator tube (MGIT). Culture for acid fast bacilli is the most specific test for TB and allows direct identification and determination of susceptibility of the causative organism A nucleic acid amplification test (NAAT), Tuberculin skin tests (TSTs), Interferon-gamma release assays (IGRAs) are commonly used as well.
Treatment The course of TB treatment depends on whether the individual is in the latent or active stage, and on his or her probability of risk. Treatment of TB usually involves a drug cocktail, or a mixture of multiple drugs, with an intensive initial 2-month phase followed by a slower 4- to 6-month continuation phase the main anti-tuberculosis drugs used in the chemotherapy of TB are: isoniazid (INH), rifampin (RIF), pyrazinamide (PZA), and either ethambutol (EMB) or streptomycin (SM). Isoniazid preventive therapy IPT is the recommended treatment for LTBI but the regimen s main drawback is the duration of therapy
Prevention The best way to prevent TB is to diagnose and isolate infectious cases rapidly and to administer appropriate treatment until patients are rendered noninfectious (usually 2 4 weeks after the start of proper treatment) and the disease is cured. Additional strategies include BCG vaccination and treatment of persons with LTBI who are at high risk of developing active disease. Mycobacterium bovis Bacillus Calmette Guérin (BCG), an attenuated vaccine derived from M. bovis, is the only licensed vaccine against tuberculosis (TB)
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