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Blood analysis shows leukopenia, thrombocytopenia and moderately elevated liver enzymes. Differential diagnosis must be made with typhus, typhoid and atypical pneumonia by Mycoplasma, Legionella or Q fever. Exposure history is paramount to diagnosis.
Diagnosis involves microbiological cultures from respiratory secretions of patients or serologically with a fourfold or greater increase in antibody titers against "C. psittaci" in blood samples combined with the probable course of the disease. Typical inclusions called "Leventhal-Cole-Lillie bodies" can be seen within macrophages in BAL (bronchoalveolar lavage) fluid. Culture of "C. psittaci" is hazardous and should only be carried out in biosafety laboratories.
Initial diagnosis may be via symptoms, but is usually confirmed via an antigen and antibody test. A PCR-based test is also available. Although any of these tests can confirm psittacosis, false negatives are possible and so a combination of clinical and lab tests is recommended before giving the bird a clean bill of health. It may die within three weeks.
Chicken respiratory diseases are difficult to differentiate and may not be diagnosed based on respiratory signs and lesions. Other diseases such as mycoplasmosis by Mycoplasma gallisepticum (chronic respiratory disease), Newcastle disease by mesogenic strains of Newcastle diseases virus (APMV-1), avian metapneumovirus, infectious laryngotracheitis, avian infectious coryza in some stages may clinically resemble IB. Similar kidney lesions may be caused by different etiologies, including other viruses, such as infectious bursal disease virus (the cause of Gumboro disease) and toxins (for instance ochratoxins of Aspergillus ochraceus), and dehydration.
In laying hens, abnormal and reduced egg production are also observed in Egg Drop Syndrome 76 (EDS), caused by an Atadenovirus and avian metapneumovirus infections. At present, IB is more common and far more spread than EDS. The large genetic and phenotypic diversity of IBV have been resulting in common vaccination failures. In addition, new strains of IBV, not present in commercial vaccines, can cause the disease in IB vaccinated flocks. Attenuated vaccines will revert to virulence by consecutive passage in chickens in densely populated areas, and may reassort with field strains, generating potentially important variants.
Definitive diagnosis relies on viral isolation and characterization. For virus characterization, recent methodology using genomic amplification (PCR) and sequencing of products, will enable very precise description of strains, according to the oligonucleotide primers designed and target gene. Methods for IBV antigens detection may employ labelled antibodies, such as direct immunofluorescence or immunoperoxidase. Antibodies to IBV may be detected by indirect immunofluorescent antibody test, ELISA and Haemagglutination inhibition (haemagglutinating IBV produced after enzymatic treatment by phospholipase C).
Although infection of avian reovirus is spread worldwide, it is rarely the sole cause of a disease. For chickens, the most common manifestation of the disease is joint/limb lameness. Confirming infection of avian reovirus can be detected through an ELISA test by using and observing the expression of σC and σB proteins. However, isolating and identifying reoviruses from tissue samples is very time consuming. Isolation is most successfully attained through inoculation of material into chick embryo cultures or fertile chicken eggs. Inoculation of embryonic eggs through the yolk sac has shown that the virus usually kills the embryos within 5 or 6 days post inoculation. Analyzing the samples, the embryos appeared hemorrhagic and necrotic lesions on the liver were present. (Jones, Onunkwo, 1978). There have also been approaches to identify avian reoviruses molecularly by observing infected tissues with dot-blot hybridization, PCR, and a combination of PCR and RFLP. This combination allows for the reovirus strain to be typed.
No specific treatment is available, but antibiotics can be used to prevent secondary infections.
Vaccines are available (ATCvet codes: for the inactivated vaccine, for the live vaccine; plus various combinations).
Biosecurity protocols including adequate isolation, disinfection are important in controlling the spread of the disease.
On chest X-ray and CT, pulmonary aspergillosis classically manifests as a halo sign, and, later, an air crescent sign.
In hematologic patients with invasive aspergillosis, the galactomannan test can make the diagnosis in a noninvasive way. False positive "Aspergillus" galactomannan tests have been found in patients on intravenous treatment with some antibiotics or fluids containing gluconate or citric acid such as some transfusion platelets, parenteral nutrition or PlasmaLyte.
On microscopy, "Aspergillus" species are reliably demonstrated by silver stains, e.g., Gridley stain or Gomori methenamine-silver. These give the fungal walls a gray-black colour. The hyphae of "Aspergillus" species range in diameter from 2.5 to 4.5 µm. They have septate hyphae, but these are not always apparent, and in such cases they may be mistaken for Zygomycota. "Aspergillus" hyphae tend to have dichotomous branching that is progressive and primarily at acute angles of about 45°.
A lumbar puncture (LP) is necessary to diagnose meningitis. Cerebrospinal fluid (CSF) culture is the most important study for the diagnosis of neonatal bacterial meningitis because clinical signs are non-specific and unreliable. Blood cultures may be negative in 15-55% of cases, deeming it unreliable as well. However, a CSF/blood glucose ratio below two-thirds has a strong relationship to bacterial meningitis. A LP should be done in all neonates with suspected meningitis, with suspected or proven sepsis (whole body inflammation) and should be considered in all neonates in whom sepsis is a possibility. The role of the LP in neonates who are healthy appearing but have maternal risk factors for sepsis is more controversial; the yield of the LP in these patients may be low.
Early-onset is deemed when infection is within one week of birth. Late-onset is deemed after the first week.
Babies born from mothers with symptoms of Herpes Simplex Virus (HSV) should be tested for viral infection. Liver tests, complete blood count (CBC), cerebrospinal fluid analyses, and chest X-ray should all be completed to diagnose meningitis. Samples should be taken from skin, conjunctiva (eye), mouth and throat, rectum, urine, and the CSF for viral culture and PCR analysis with respect to the sample from CSF.
Patients with symptoms of CAP require evaluation. Diagnosis of pneumonia is made clinically, rather than on the basis of a particular test. Evaluation begins with a physical examination by a health provider, which may reveal fever, an increased respiratory rate (tachypnea), low blood pressure (hypotension), a fast heart rate (tachycardia) and changes in the amount of oxygen in the blood. Palpating the chest as it expands and tapping the chest wall (percussion) to identify dull, non-resonant areas can identify stiffness and fluid, signs of CAP. Listening to the lungs with a stethoscope (auscultation) can also reveal signs associated with CAP. A lack of normal breath sounds or the presence of crackles can indicate fluid consolidation. Increased vibration of the chest when speaking, known as tactile fremitus, and increased volume of whispered speech during auscultation can also indicate fluid.
When signs of pneumonia are discovered during evaluation, chest X-rays, are performed to support a diagnosis of CAP, and examination of the blood and sputum for infectious microorganisms and blood tests may be used to support a diagnosis of CAP. Diagnostic tools depend on the severity of illness, local practices and concern about complications of the infection. All patients with CAP should have their blood oxygen monitored with pulse oximetry. In some cases, arterial blood gas analysis may be required to determine the amount of oxygen in the blood. A complete blood count (CBC) may reveal extra white blood cells, indicating infection.
Chest X-rays and X-ray computed tomography (CT) can reveal areas of opacity (seen as white), indicating consolidation. CAP does not always appear on x-rays, because the disease is in its initial stages or involves a part of the lung an x-ray does not see well. In some cases, chest CT can reveal pneumonia not seen on x-rays. However, congestive heart failure or other types of lung damage can mimic CAP on x-rays.
Several tests can identify the cause of CAP. Blood cultures can isolate bacteria or fungi in the bloodstream. Sputum Gram staining and culture can also reveal the causative microorganism. In severe cases, bronchoscopy can collect fluid for culture. Special tests can be performed if an uncommon microorganism is suspected, such as urinalysis for Legionella antigen in Legionnaires' disease.
Other conditions that may mimic cellulitis include deep vein thrombosis, which can be diagnosed with a compression leg ultrasound, and stasis dermatitis, which is inflammation of the skin from poor blood flow. Signs of a more severe infection such as necrotizing fasciitis or gas gangrene that would require prompt surgical intervention include purple bullae, skin sloughing, subcutaneous edema, and systemic toxicity. Misdiagnosis can occur in up to 30% of people with suspected lower-extremity cellulitis, leading to 50,000 to 130,000 unnecessary hospitalization and $195 to $515 million in avoidable healthcare spending annually in the United States.
Associated musculoskeletal findings are sometimes reported. When it occurs with acne conglobata, hidradenitis suppurativa, and pilonidal cysts, the syndrome is referred to as the follicular occlusion triad or tetrad.
Lyme disease can be misdiagnosed as staphylococcal- or streptococcal-induced cellulitis. Because the characteristic bullseye rash does not always appear in people infected with Lyme disease, the similar set of symptoms may be misdiagnosed as cellulitis. Standard treatments for cellulitis are not sufficient for curing Lyme disease. The only way to rule out Lyme disease is with a blood test, which is recommended during warm months in areas where the disease is endemic.
In those who have previously had cellulitis, the use of antibiotics may help prevent future episodes. This is recommended by CREST for those who have had more than two episodes.
Some ways to prevent airborne diseases include washing hands, using appropriate hand disinfection, getting regular immunizations against diseases believed to be locally present, wearing a respirator and limiting time spent in the presence of any patient likely to be a source of infection.
Exposure to a patient or animal with an airborne disease does not guarantee receiving the disease. Because of the changes in host immunity and how much the host was exposed to the particles in the air makes a difference to how the disease affects the body.
Antibiotics are not prescribed for patients to control viral infections. They may however be prescribed to a flu patient for instance, to control or prevent bacterial secondary infections. They also may be used in dealing with air-borne bacterial primary infections, such as pneumonic plague.
Additionally the Centers for Disease Control and Prevention (CDC) has told consumers about vaccination and following careful hygiene and sanitation protocols for airborne disease prevention. Consumers also have access to preventive measures like UV Air purification devices that FDA and EPA-certified laboratory test data has verified as effective in inactivating a broad array of airborne infectious diseases. Many public health specialists recommend social distancing to reduce the transmission of airborne infections.
Cats can be protected from H5N1 if they are given a vaccination, as mentioned above. However, it was also found that cats can still shed some of the virus but in low numbers.
If a cat is exhibiting symptoms, they should be put into isolation and kept indoors. Then they should be taken to a vet to get tested for the presence of H5N1. If there is a possibility that the cat has Avian Influenza, then there should be extra care when handling the cat. Some of the precautions include avoiding all direct contact with the cat by wearing gloves, masks, and goggles. Whatever surfaces the cat comes in contact with should be disinfected with standard household cleaners.
They have given tigers an antiviral treatment of Oseltamivir with a dose of 75 mg/60 kg two times a day. The specific dosage was extrapolated from human data, but there hasn't been any data to suggest protection. As with many antiviral treatments, the dosage depends on the species.
Although the presentation of scarlet fever can be clinically diagnosed, further testing may be required to distinguish it from other illnesses. Also, history of a recent exposure to someone with strep throat can be useful. There are two methods used to confirm suspicion of scarlet fever rapid antigen detection test and throat culture.
The rapid antigen detection test is a very specific test but not very sensitive. This means that if the result is positive (indicating that the Group A Strep Antigen was detected and therefore confirming that the patient has a Group A Strep Pharyngitis) then it is appropriate to treat them with antibiotics. However, if the Rapid Antigen Detection Test is negative (indicating that they do not have Group A Strep Pharyngitis), then a throat culture is required to confirm since it could be a false negative result. The throat culture is the current gold standard for diagnosis.
Serologic testing looks for the antibodies that the body produces against the streptococcal infection including antistreptolysin-O and antideoxyribonuclease B. It takes the body 2–3 weeks to make these antibodies so this type of testing is not useful for diagnosing a current infection. However, it is useful when assessing a patient who may have one of the complications from a previous streptococcal infection.
Throat cultures done after antibiotic therapy can tell you if the infection has been removed. These throat swabs however are not indicated because up to 25% of properly treated individuals can continue to carry the streptococcal infection while asymptomatic.
CAP is treated with an antibiotic that kills the offending microorganism and by managing complications. If the causative microorganism is unidentified (often the case), the laboratory identifies the most-effective antibiotic; this may take several days.
Health professionals consider a person's risk factors for various organisms when choosing an initial antibiotic. Additional consideration is given to the treatment setting; most patients are cured by oral medication, while others must be hospitalized for intravenous therapy or intensive care.
Therapy for older children and adults generally includes treatment for atypical bacteria: typically a macrolide antibiotic (such as azithromycin or clarithromycin) or a quinolone, such as levofloxacin. Doxycycline is the antibiotic of choice in the UK for atypical bacteria, due to increased clostridium difficile colitis in hospital patients linked to the increased use of clarithromycin.
Vaccines are available (ATCvet codes: for the inactivated vaccine, for the live vaccine, plus various combinations).
Given that avian reovirus infections are widespread, the viruses are relatively resistant outside the host, and that vertical and horizontal transmission occurs, eradicating avian reovirus infection in commercial chicken flocks is very unlikely. In addition, absence of detectable seroconversion and failure to detect virus in cloacal swabs are unreliable indicators of resisting infection, or transmission via the egg. Thus, the most proactive and successful approach to controlling this disease is through vaccination. Since chicks are more prone to being detrimentally affected by the disease right after hatching, vaccine protocols that use live and killed vaccines are designed to provide protection during the very early stages of life. This approach has been accomplished through active immunity after early vaccination and a live vaccine or passive immunity from maternal antibodies followed with vaccination of the breeder hens. Currently, efforts toward administering inactivated or live vaccines to breeding stock to allow passive immunity to the offspring via the yolk are being taken.
"Other infections include:"
- "Closed-space infections of the fingertips, known as paronychia."
At the start of each wrestling meet, trained referees examine the skin of all wrestlers before any participation. During this examination, male wrestlers are to wear shorts; female wrestlers are only permitted to wear shorts and a sports bra. Open wounds and infectious skin conditions that cannot be adequately protected are considered grounds for disqualification from both practice and competition. This essentially means that the skin condition has been deemed as non-infectious and adequately medicated, covered with a tight wrapping and proper ointment. In addition, the wrestler must have developed no new lesions in the 72 hours before the examination. Wrestlers who are undergoing treatment for a communicable skin disease at the time of the meet or tournament shall provide written documentation to that effect from a physician. This documentation should include the wrestler’s diagnosis, culture results (if possible), date and time therapy began, and the exact names of medication for treatment. These measures aren’t always successful, and the infection is sometimes spread regardless.
"Staphylococcus" is a genus of Gram-positive bacteria that can cause a wide variety of infections in humans and other animals through infection or the production of toxins.
Staphylococcal toxins are a common cause of food poisoning, as they can be produced in improperly-stored food. Staphylococci are also known to be a cause of bacterial conjunctivitis. "Staphylococcus aureus" can cause a number of different skin diseases. Among neurosurgical patients, it can cause community-acquired meningitis.
The presence of avian botulism is extremely hard to detect before an outbreak. Frequent surveillance of sites at risk is needed for early detection of the disease in order to take action and remove carcasses. Vaccines are also developed, but they are expected to have limited effectiveness in stemming outbreaks in wild waterbird populations. However may be effective in reducing mortality for endangered island waterfowl and small non-migratory wild populations. Field tests are needed.
The diagnosis of SSSS is made clinically. This is sometimes confirmed by isolation of "S. aureus" from blood, mucous membranes, or skin biopsy; however, these are often negative. Skin biopsy may show separation of the superficial layer of the epidermis (intraepidermal separation), differentiating SSSS from TEN, wherein the separation occurs at the dermo-epidermal junction (subepidermal separation). SSSS may be difficult to distinguish from toxic epidermal necrolysis and pustular psoriasis.
Methicillin-resistant Staphylococcus aureus (MRSA) evolved from Methicillin-susceptible Staphylococcus aureus (MSSA) otherwise known as common "S. aureus". Many people are natural carriers of "S. aureus", without being affected in any way. MSSA was treatable with the antibiotic methicillin until it acquired the gene for antibiotic resistance. Though genetic mapping of various strains of MRSA, scientists have found that MSSA acquired the mecA gene in the 1960s, which accounts for its pathogenicity, before this it had a predominantly commensal relationship with humans. It is theorized that when this "S. aureus" strain that had acquired the mecA gene was introduced into hospitals, it came into contact with other hospital bacteria that had already been exposed to high levels of antibiotics. When exposed to such high levels of antibiotics, the hospital bacteria suddenly found themselves in an environment that had a high level of selection for antibiotic resistance, and thus resistance to multiple antibiotics formed within these hospital populations. When "S. aureus" came into contact with these populations, the multiple genes that code for antibiotic resistance to different drugs were then acquired by MRSA, making it nearly impossible to control. It is thought that MSSA acquired the resistance gene through the horizontal gene transfer, a method in which genetic information can be passed within a generation, and spread rapidly through its own population as was illustrated in multiple studies. Horizontal gene transfer speeds the process of genetic transfer since there is no need to wait an entire generation time for gene to be passed on. Since most antibiotics do not work on MRSA, physicians have to turn to alternative methods based in Darwinian medicine. However prevention is the most preferred method of avoiding antibiotic resistance. By reducing unnecessary antibiotic use in human and animal populations, antibiotics resistance can be slowed.
The current medical treatments for aggressive invasive aspergillosis include voriconazole and liposomal amphotericin B in combination with surgical debridement.
For the less aggressive allergic bronchopulmonary aspergillosis findings suggest the use of oral steroids for a prolonged period of time, preferably for 6–9 months in allergic aspergillosis of the lungs. Itraconazole is given with the steroids, as it is considered to have a "steroid sparing" effect, causing the steroids to be more effective, allowing a lower dose.,
Other drugs used, such as amphotericin B, caspofungin (in combination therapy only), flucytosine (in combination therapy only), or itraconazole,
are used to treat this fungal infection. However, a growing proportion of infections are resistant to the triazoles. "A. fumigatus", the most commonly infecting species, is intrinsically resistant to fluconazole.
According to the NCAA Wrestling Rules and Interpretations, used by all high schools in the United States: "Infection control measures, or measures that seek to prevent the spread of disease, should be utilized to reduce the risks of disease transmission. Efforts should be made to improve wrestler hygiene practices, to utilize recommended procedures for cleaning and disinfection of surfaces, and to handle blood and other bodily fluids appropriately. Suggested measures include: promotion of hand hygiene practices; educating athletes not to pick, squeeze, or scratch skin lesions; encouraging athletes to shower after activity; educating athletes not to share protective gear, towels, razors or water bottles; ensuring recommended procedures for cleaning and disinfection of wrestling mats, all athletic equipment, locker rooms, and whirlpool tubs are closely followed; and verifying clean up of blood and other potentially infectious materials." More ways of prevention include wearing long sleeve shirts and sweatpants to limit
the amount of skin to skin contact. A wrestler should also not share their
equipment with other teammates and should regularly check their skin for any lesions or other signs of outbreaks. Body wipes are also common to see Coaches must also enforce the disinfecting and sanitary cleansing of the wrestling mats and other practice areas. This can greatly limit the spread of skin infections that can infect an individual indirectly.
One high school wrestling coach from Southern California described his methods of prevention using three simple procedures. “Keep the mats [clean]…you’ve got to bleach and mop them every day before practice. Along the same lines, gear should also be washed regularly, especially headgear…Most importantly, the wrestlers need to shower immediately after practices. If one kid doesn’t, and he gets [infected], it can spread to everyone else on the team within a week. I’ve had it happen before, to the point where some schools won’t allow any of our guys to wrestle in a meet. When this happens, it’s a huge blow to the school’s record and reputation. In the future, we are less likely to be invited to exclusive tournaments in the coming year.”
Diagnosis of lymphoid tumors in poultry is complicated due to multiple etiological agents capable of causing very similar tumors. It is not uncommon that more than one avian tumor virus can be present in a chicken, thus one must consider both the diagnosis of the disease/tumors (pathological diagnosis) and of the virus (etiological diagnosis). A step-wise process has been proposed for diagnosis of Marek’s disease which includes (1) history, epidemiology, clinical observations and gross necropsy, (2) characteristics of the tumor cell, and (3) virological characteristics
The demonstration of peripheral nerve enlargement along with suggestive clinical signs in a bird that is around three to four months old (with or without visceral tumors) is highly suggestive of Marek's disease. Histological examination of nerves reveals infiltration of pleomorphic neoplastic and inflammatory lymphocytes. Peripheral neuropathy should also be considered as a principal rule-out in young chickens with paralysis and nerve enlargement without visceral tumors, especially in nerves with interneuritic edema and infiltration of plasma cells.
The presence of nodules on the internal organs may also suggest Marek's disease, but further testing is required for confirmation. This is done through histological demonstration of lymphomatous infiltration into the affected tissue. A range of leukocytes can be involved, including lymphocytic cell lines such as large lymphocyte, lymphoblast, primitive reticular cells, and occasional plasma cells, as well as macrophage and plasma cells. The T cells are involved in the malignancy, showing neoplastic changes with evidence of mitosis. The lymphomatous infiltrates need to be differentiated from other conditions that affect poultry including lymphoid leukosis and reticuloendotheliosis, as well as an inflammatory event associated with hyperplastic changes of the affected tissue.
Key clinical signs as well as gross and microscopic features that are most useful for differentiating Marek’s disease from lymphoid leukosis and reticuloendotheliosis include (1) Age: MD can affect birds at any age, including 5% in unvaccinated flocks; (4) Potential nerve enlargement; (5) Interfollicular tumors in the bursa of Fabricius; (6) CNS involvement; (7) Lymphoid proliferation in skin and feather follicles; (8) Pleomorphic lymphoid cells in nerves and tumors; and (9) T-cell lymphomas.
In addition to gross pathology and histology, other advanced procedures used for a definitive diagnosis of Marek’s disease include immunohistochemistry to identify cell type and virus-specific antigens, standard and quantitative PCR for identification of the virus, virus isolation to confirm infections, and serology to confirm/exclude infections.
The World Organisation for Animal Health (OIE) reference laboratories for Marek’s disease include the Pirbright Institute, UK and the USDA Avian Disease and Oncology Laboratory, USA.