Currently, there is no proven, safe treatment for monkeypox. The people who have been infected can be vaccinated up to 14 days after exposure.

Lesions of paravaccinia virus will clear up with little to no scaring after 4 to 8 weeks. An antibiotic may be prescribed by a physician to help prevent bacterial infection of the lesion area. In rare cases, surgical removal of the lesions can be done to help increase rate of healing, and help minimize risk of bacterial or fungal infection. Upon healing, no long term side effects have been reported.

Diagnosis of paravaccinia virus will often come from Polymerase chain reaction screening ordered by their physician. However, due to how common paravaccinia virus is in rural areas, individuals typically do not seek professional help in diagnosis. Instead individuals may refer to people with local knowledge of the cattle in their area such as ranchers, or veterinarians who have some familiarity with the infections in the region.

Variola caprina (goat pox) is a contagious viral disease caused by a pox virus that affects goats. The virus usually spreads via the respiratory system, and sometimes spreads through abraded skin. It is most likely to occur in crowded stock. Sources of the virus include cutaneous lesions, saliva, nasal secretions and faeces. There are two types of the disease: the papulo-vesicular form and the nodular form (stone pox). The incubation period is usually 8–13 days, but it may be as short as four days.

It is thought the same virus spreads sheep pox, to which European sheep breeds are highly susceptible. The virus may be present in dried scabs for up to six months.

In endemic areas the morbidity rate is 70–90% and the mortality rate is 5–10%. The mortality rate may reach nearly 100% in imported animals. Resistant animals may show only a mild form of the disease, which may be missed as only a few lesions are present, usually around the ears or the tail.

Vaccination against smallpox is assumed to provide protection against human monkeypox infection considering they are closely related viruses and the vaccine protects animals from experimental lethal monkeypox challenge. This has not been conclusively demonstrated in humans because routine smallpox vaccination was discontinued following the apparent eradication of smallpox and due to safety concerns with the vaccine.

Smallpox vaccine has been reported to reduce the risk of monkeypox among previously vaccinated persons in Africa. The decrease in immunity to poxviruses in exposed populations is a factor in the prevalence of monkeypox. It is attributed both to waning cross-protective immunity among those vaccinated before 1980 when mass smallpox vaccinations were discontinued, and to the gradually increasing proportion of unvaccinated individuals. The United States Centers for Disease Control and Prevention (CDC) recommends that persons investigating monkeypox outbreaks and involved in caring for infected individuals or animals should receive a smallpox vaccination to protect against monkeypox. Persons who have had close or intimate contact with individuals or animals confirmed to have monkeypox should also be vaccinated.

CDC does not recommend preexposure vaccination for unexposed veterinarians, veterinary staff, or animal control officers, unless such persons are involved in field investigations.

It has been recorded since the late 19th century and has been reported from most sheep-or goat-raising areas including those in Europe, the Middle East, the United States, Africa, Asia, Alaska, South America, Canada, New Zealand and Australia. Orf is spread by fomites and direct contact. In some environments infection is injected by scratches from thistles of both growing and felled plants. Symptoms include papules and pustules on the lips and muzzle, and less commonly in the mouth of young lambs and on the eyelids, feet, and teats of ewes. The lesions progress to thick crusts which may bleed. Orf in the mouths of lambs may prevent suckling and cause weight loss, and can infect the udder of the mother ewe, thus potentially leading to mastitis. Sheep are prone to reinfection. Occasionally the infection can be extensive and persistent if the animal does not produce an immune response.

A live virus vaccine (ATCvet code: ) is made from scab material and usually given to ewes at the age of two months, but only to lambs when there is an outbreak. The vaccine can cause disease in humans.

In sheep and goats the lesions mostly appear on or near the hairline and elsewhere on the lips and muzzle. In some cases the lesions appear on and in the nostrils, around the eyes, on the thigh, coronet, vulva, udder and axilla. In rare cases, mostly involving young lambs, lesions are found on the tongue, gums, roof of the mouth and the oesophagus. It has also been reported a number of times to cause lesions in the rumen. In one case it was shown that a severe form of orf virus caused an outbreak involving the gastrointestinal tract, lungs, heart, as well as the buccal cavity, cheeks, tongue and lips. Another severe case was reported pharyngitis, genital lesions and infection of the hooves which led to lameness and, in some cases, sloughing of the hoof.

More typically sheep will become free of orf within a week or so as the disease runs its course. Sheep custodians can assist by ensuring infected lambs receive sufficient milk and separating out the infected stock to slow down cross-transmission to healthy animals. It is advisable for those handling infected animals to wear disposable gloves to prevent cross-infection and self-infection. A veterinarian needs to be contacted if there is a risk of misdiagnosis with other, more serious conditions.

Goat pox is found in the part of Africa north of the equator, the Middle East, Central Asia and India. It may be spread between animals by:

- Direct contact

- Indirect transmission by contaminated implements, vehicles or products such as litter or fodder

- Indirect transmission by insects (mechanical vectors).

- Contamination by inhalation, intradermal or subcutaneous inoculation, or by respiratory, transcutaneous and transmucosal routes

Orf is a zoonotic disease, meaning humans can contract this disorder through direct contact with infected sheep and goats or with fomites carrying the orf virus. It causes a purulent-appearing papule locally and generally no systemic symptoms. Infected locations can include the finger, hand, arm, face and even the penis (caused by infection either from the hand during urination or from bestiality). Consequently, it is important to observe good personal hygiene and to wear gloves when treating infected animals. The papule may persist for 7 to 10 weeks and spontaneously resolves. It is an uncommon condition and may be difficult to diagnose.

While orf is usually a benign self-limiting illness, it can be very progressive and even life-threatening in the immune-compromised host. One percent topical cidofovir has been successfully used in a few patients with progressive disease. Serious damage may be inflicted on the eye if it is infected by orf, even among healthy individuals. The virus can survive in the soil for at least six months.

The clinical definition of smallpox is an illness with acute onset of fever equal to or greater than followed by a rash characterized by firm, deep seated vesicles or pustules in the same stage of development without other apparent cause. If a clinical case is observed, smallpox is confirmed using laboratory tests.

Microscopically, poxviruses produce characteristic cytoplasmic inclusions, the most important of which are known as Guarnieri bodies, and are the sites of viral replication. Guarnieri bodies are readily identified in skin biopsies stained with hematoxylin and eosin, and appear as pink blobs. They are found in virtually all poxvirus infections but the absence of Guarnieri bodies cannot be used to rule out smallpox. The diagnosis of an orthopoxvirus infection can also be made rapidly by electron microscopic examination of pustular fluid or scabs. All orthopoxviruses exhibit identical brick-shaped virions by electron microscopy. If particles with the characteristic morphology of herpesviruses are seen this will eliminate smallpox and other orthopoxvirus infections.

Definitive laboratory identification of variola virus involves growing the virus on chorioallantoic membrane (part of a chicken embryo) and examining the resulting pock lesions under defined temperature conditions. Strains may be characterized by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) analysis. Serologic tests and enzyme linked immunosorbent assays (ELISA), which measure variola virus-specific immunoglobulin and antigen have also been developed to assist in the diagnosis of infection.

Chickenpox was commonly confused with smallpox in the immediate post-eradication era. Chickenpox and smallpox can be distinguished by several methods. Unlike smallpox, chickenpox does not usually affect the palms and soles. Additionally, chickenpox pustules are of varying size due to variations in the timing of pustule eruption: smallpox pustules are all very nearly the same size since the viral effect progresses more uniformly. A variety of laboratory methods are available for detecting chickenpox in evaluation of suspected smallpox cases.

The simplest procedure for 'in field diagnosis' is the detection of antibodies by latex agglutination (LAT) as it is quick and simple to run, and has a long shelf-life. Other procedures used for diagnosis include growth inhibition disc tests (GI), direct and indirect fluorescent antibody tests, complement fixation tests (CFT), indirect haemagglutination test (IHA), ELISA and PCR. These have varying degrees of efficacy.

Isolation of "M. capricolum "subsp. "capripneumoniae" from clinical samples is the only way to definitively diagnose the infection but it is not normally performed as it is time consuming and difficult.

Alastrim, also known as variola minor, was the milder strain of the variola virus that caused smallpox. The last known case of variola minor was in Somalia, Africa in 1977. Smallpox was formally declared eradicated in May 1980.

Variola minor is of the genus orthopoxvirus, which are DNA viruses that replicate in the cytoplasm of the affected cell, rather than in its nucleus. Like variola major, alastrim was spread through inhalation of the virus in the air, which could occur through face-to-face contact or through fomites. Infection with variola minor conferred immunity against the more dangerous variola major.

Variola minor was a less common form of the virus, and much less deadly. Although alastrim had the same incubation period and pathogenetic stages as smallpox, alastrim is believed to have had a mortality rate of less than 1%, as compared to smallpox's 30%.

Because alastrim was a less debilitating disease than smallpox, patients were more frequently ambulant and thus able to infect others more rapidly. As such, variola minor swept through the USA, Great Britain, and South Africa in the early 20th century, becoming the dominant form of the disease in those areas and thus rapidly decreasing mortality rates.

Alastrim was also called white pox, kaffir pox, Cuban itch, West Indian pox, milk pox, and pseudovariola.

Like smallpox, alastrim has now been totally eradicated from the globe thanks to the 1960s Global Smallpox Eradication campaign. The last case of indigenous variola minor was reported in a Somalian cook, Ali Maow Maalin, in October 1977, and smallpox was officially declared eradicated worldwide in May 1980.

Key measures to prevent outbreaks of the disease are maintaining hygiene standards and using screening to exclude persons with suspicious infections from engaging in contact sports. A skin check performed before practice or competition takes place can identify individuals who should be evaluated, and if necessary treated by a healthcare professional. In certain situations, i.e. participating in wrestling camps, consider placing participants on valacyclovir 1GM daily for the duration of camp. 10-year study has shown 89.5% reduction in outbreaks and probable prevention of contracting the virus. Medication must be started 5 days before participation to ensure proper concentrations exist.

Pigeon pox is a viral disease to which pigeons are susceptible. There is a live viral vaccine available (ATCvet code: ). Pigeon pox is caused by a virus that is spread by mosquitoes and dirty water but not in droppings.

Various techniques may be used for the direct identification of "B. anthracis" in clinical material. Firstly, specimens may be Gram stained. "Bacillus" spp. are quite large in size (3 to 4 μm long), they may grow in long chains, and they stain Gram-positive. To confirm the organism is "B. anthracis", rapid diagnostic techniques such as polymerase chain reaction-based assays and immunofluorescence microscopy may be used.

All "Bacillus" species grow well on 5% sheep blood agar and other routine culture media. Polymyxin-lysozyme-EDTA-thallous acetate can be used to isolate "B. anthracis" from contaminated specimens, and bicarbonate agar is used as an identification method to induce capsule formation. "Bacillus" spp. usually grow within 24 hours of incubation at 35°C, in ambient air (room temperature) or in 5% CO. If bicarbonate agar is used for identification, then the medium must be incubated in 5% CO. "B. anthracis" colonies are medium-large, gray, flat, and irregular with swirling projections, often referred to as having a "medusa head" appearance, and are not hemolytic on 5% sheep blood agar. The bacteria are not motile, susceptible to penicillin, and produce a wide zone of lecithinase on egg yolk agar. Confirmatory testing to identify "B. anthracis" includes gamma bacteriophage testing, indirect hemagglutination, and enzyme-linked immunosorbent assay to detect antibodies. The best confirmatory precipitation test for anthrax is the Ascoli test.

Cowpox originates on the udders or teats of cows. It is classified as a zoonotic disease, which means it can be transferred from animals to humans and vice versa. Cowpox is an infectious disease. So, the disease can manifest on cows in environments where bacteria thrive, due to unsanitary conditions, or randomly. Cowpox symptoms are similar in whichever host they infect: cow, cat, human. Cowpox symptoms include round, pus filled lesions on the skin at the site of infection. In most cases of humans, the lesions develop on the inner and outer parts of the hand and fingers. In some cases, the infected person can develop a mild fever or inflammation around the lesions. Cowpox can be transferred from human to human by contact of the infected site to another individual. It is very similar in pathology and structure in contrast to small pox. However, cowpox has increased activity in between the ectoderm and endoderm layers of the human skin. Cowpox includes both A type bodies and B type inclusion bodies which largely impacts the pathology of the disease.

The diagnosis of chickenpox is primarily based on the signs and symptoms, with typical early symptoms followed by a characteristic rash. Confirmation of the diagnosis is by examination of the fluid within the vesicles of the rash, or by testing blood for evidence of an acute immunologic response.

Vesicular fluid can be examined with a Tzanck smear, or by testing for direct fluorescent antibody. The fluid can also be "cultured", whereby attempts are made to grow the virus from a fluid sample. Blood tests can be used to identify a response to acute infection (IgM) or previous infection and subsequent immunity (IgG).

Prenatal diagnosis of fetal varicella infection can be performed using ultrasound, though a delay of 5 weeks following primary maternal infection is advised. A PCR (DNA) test of the mother's amniotic fluid can also be performed, though the risk of spontaneous abortion due to the amniocentesis procedure is higher than the risk of the baby's developing fetal varicella syndrome.

Eczema vaccinatum is a serious medical condition that requires immediate and intensive medical care. Therapy has been supportive, such as antibiotics, fluid replacement, antipyretics and analgesics, skin healing, etc.; vaccinia immune globulin (VIG) could be very useful but supplies may be deficient as of 2006. Antiviral drugs have been examined for activity in pox viruses and cidofovir is believed to display potential in this area.

Cowpox is an infectious disease caused by the cowpox virus. The virus, part of the orthopoxvirus family, is closely related to the "vaccinia" virus. The virus is zoonotic, meaning that it is transferable between species, such as from animal to human. The transferral of the disease was first observed in dairymaids who touched the udders of infected cows and consequently developed the signature pustules on their hands. Cowpox is more commonly found in animals other than bovines, such as rodents. Cowpox is similar to, but much milder than, the highly contagious and often deadly smallpox disease. Its close resemblance to the mild form of smallpox and the observation that dairymaids were immune from smallpox inspired the first smallpox vaccine, created and administered by English physician Edward Jenner.

The word “vaccination,” coined by Jenner in 1796, is derived from the Latin root "vaccinus", meaning of or from the cow. Once vaccinated, a patient develops antibodies that make them immune to cowpox, but they also develop immunity to the smallpox virus, or "Variola virus". The cowpox vaccinations and later incarnations proved so successful that in 1980, the World Health Organization announced that smallpox was the first disease to be eradicated by vaccination efforts worldwide. Other orthopox viruses remain prevalent in certain communities and continue to infect humans, such as the cowpox virus (CPXV) in Europe, vaccinia in Brazil, and monkeypox virus in Central and West Africa.

MAP is capable of causing Johne's-like symptoms in humans, though difficulty in testing for MAP infection presents a diagnostic hurdle.

Clinical similarities are seen between Johne's disease in ruminants and inflammatory bowel disease in humans, and because of this, some researchers contend the organism is a cause of Crohn's disease. However, epidemiologic studies have provided variable results; in certain studies, the organism (or an immune response directed against it) has been much more frequently found in patients with Crohn's disease than asymptomatic people.

If a person is suspected as having died from anthrax, precautions should be taken to avoid skin contact with the potentially contaminated body and fluids exuded through natural body openings. The body should be put in strict quarantine. A blood sample should then be collected and sealed in a container and analyzed in an approved laboratory to ascertain if anthrax is the cause of death. Then, the body should be incinerated. Microscopic visualization of the encapsulated bacilli, usually in very large numbers, in a blood smear stained with polychrome methylene blue (McFadyean stain) is fully diagnostic, though culture of the organism is still the gold standard for diagnosis. Full isolation of the body is important to prevent possible contamination of others. Protective, impermeable clothing and equipment such as rubber gloves, rubber apron, and rubber boots with no perforations should be used when handling the body. No skin, especially if it has any wounds or scratches, should be exposed. Disposable personal protective equipment is preferable, but if not available, decontamination can be achieved by autoclaving. Disposable personal protective equipment and filters should be autoclaved, and/or burned and buried. Anyone working with anthrax in a suspected or confirmed person should wear respiratory equipment capable of filtering particles of their size or smaller. The US National Institute for Occupational Safety and Health – and Mine Safety and Health Administration-approved high-efficiency respirator, such as a half-face disposable respirator with a high-efficiency particulate air filter, is recommended. All possibly contaminated bedding or clothing should be isolated in double plastic bags and treated as possible biohazard waste. The body of an infected person should be sealed in an airtight body bag. Dead people who are opened and not burned provide an ideal source of anthrax spores. Cremating people is the preferred way of handling body disposal. No embalming or autopsy should be attempted without a fully equipped biohazard laboratory and trained, knowledgeable personnel.

Herpes outbreaks should be treated with antiviral medications like Acyclovir, Valacyclovir, or Famcyclovir, each of which is available in tablet form.

Oral antiviral medication is often used as a prophylactic to suppress or prevent outbreaks from occurring. The recommended dosage for suppression therapy for recurrent outbreaks is 1,000 mg of valacyclovir once a day or 400 mg Acyclovir taken twice a day. In addition to preventing outbreaks, these medications greatly reduce the chance of infecting someone while the patient is not having an outbreak.

Often, people have regular outbreaks of anywhere from 1 to 10 times per year, but stress (because the virus lies next to the nerve cells), or a weakened immune system due to a temporary or permanent illness can also spark outbreaks. Some people become infected but fail to ever have a single outbreak, although they remain carriers of the virus and can pass the disease on to an uninfected person through asymptomatic shedding (when the virus is active on the skin but rashes or blisters do not appear).

The use of antiviral medications has been shown to be effective in preventing acquisition of the herpes virus. Specific usage of these agents focus on wrestling camps where intense contact between individuals occur on a daily basis over several weeks. They have also been used for large outbreaks during seasonal competition, but further research needs to be performed to verify efficacy.

Recommendations for the diagnosis of congenital toxoplasmosis include: prenatal diagnosis based on testing of amniotic fluid and ultrasound examinations; neonatal diagnosis based on molecular testing of placenta and cord blood and comparative mother-child serologic tests and a clinical examination at birth; and early childhood diagnosis based on neurologic and ophthalmologic examinations and a serologic survey during the first year of life. During pregnancy, serological testing is recommended at three week intervals.

Even though diagnosis of toxoplasmosis heavily relies on serological detection of specific anti-"Toxoplasma" immunoglobulin, serological testing has limitations. For example, it may fail to detect the active phase of "T. gondii" infection because the specific anti-"Toxoplasma" IgG or IgM may not be produced until after several weeks of infection. As a result, a pregnant woman might test negative during the active phase of "T. gondii" infection leading to undetected and therefore untreated congenital toxoplasmosis. Also, the test may not detect "T. gondii" infections in immunocompromised patients because the titers of specific anti-"Toxoplasma" IgG or IgM may not rise in this type of patient.

Many PCR-based techniques have been developed to diagnose toxoplasmosis using clinical specimens that include amniotic fluid, blood, cerebrospinal fluid, and tissue biopsy. The most sensitive PCR-based technique is nested PCR, followed by hybridization of PCR products. The major downside to these techniques is that they are time consuming and do not provide quantitative data.

Real-time PCR is useful in pathogen detection, gene expression and regulation, and allelic discrimination. This PCR technique utilizes the 5' nuclease activity of "Taq" DNA polymerase to cleave a nonextendible, fluorescence-labeled hybridization probe during the extension phase of PCR. A second fluorescent dye, e.g., 6-carboxy-tetramethyl-rhodamine, quenches the fluorescence of the intact probe. The nuclease cleavage of the hybridization probe during the PCR releases the effect of quenching resulting in an increase of fluorescence proportional to the amount of PCR product, which can be monitored by a sequence detector.

Toxoplasmosis cannot be detected with immunostaining. Lymph nodes affected by "Toxoplasma" have characteristic changes, including poorly demarcated reactive germinal centers, clusters of monocytoid B cells, and scattered epithelioid histiocytes.

The classic triad of congenital toxoplasmosis includes: chorioretinitis, hydrocephalus, and intracranial artheriosclerosis.

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.

An emerging infectious disease (EID) is an infectious disease whose incidence has increased in the past 20 years and could increase in the near future. Emerging infections account for at least 12% of all human pathogens. EIDs are caused by newly identified species or strains (e.g. Severe acute respiratory syndrome, HIV/AIDS) that may have evolved from a known infection (e.g. influenza) or spread to a new population (e.g. West Nile fever) or to an area undergoing ecologic transformation (e.g. Lyme disease), or be "reemerging" infections, like drug resistant tuberculosis. Nosocomial (hospital-acquired) infections, such as methicillin-resistant Staphylococcus aureus are emerging in hospitals, and extremely problematic in that they are resistant to many antibiotics. Of growing concern are adverse synergistic interactions between emerging diseases and other infectious and non-infectious conditions leading to the development of novel syndemics. Many emerging diseases are zoonotic - an animal reservoir incubates the organism, with only occasional transmission into human populations.

Diagnosis of toxoplasmosis in humans is made by biological, serological, histological, or molecular methods, or by some combination of the above. Toxoplasmosis can be difficult to distinguish from primary central nervous system lymphoma. It mimics several other infectious diseases so clinical signs are non-specific and are not sufficiently characteristic for a definite diagnosis. As a result, the diagnosis is made by a trial of therapy (pyrimethamine, sulfadiazine, and folinic acid (USAN: leucovorin)), if the drugs produce no effect clinically and no improvement on repeat imaging.

"T. gondii" may also be detected in blood, amniotic fluid, or cerebrospinal fluid by using polymerase chain reaction. "T. gondii" may exist in a host as an inactive cyst that would likely evade detection.

Serological testing can detect "T. gondii" antibodies in blood serum, using methods including the Sabin–Feldman dye test (DT), the indirect hemagglutination assay, the indirect fluorescent antibody assay (IFA), the direct agglutination test, the latex agglutination test (LAT), the enzyme-linked immunosorbent assay (ELISA), and the immunosorbent agglutination assay test (IAAT).

The most commonly used tests to measure IgG antibody are the DT, the ELISA, the IFA, and the modified direct agglutination test. IgG antibodies usually appear within a week or two of infection, peak within one to two months, then decline at various rates. "Toxoplasma" IgG antibodies generally persist for life, and therefore may be present in the bloodstream as a result of either current or previous infection.

To some extent, acute toxoplasmosis infections can be differentiated from chronic infections using an IgG avidity test, which is a variation on the ELISA. In the first response to infection, toxoplasma-specific IgG has a low affinity for the toxoplasma antigen; in the following weeks and month, IgG affinity for the antigen increases. Based on the IgG avidity test, if the IgG in the infected individual has a high affinity, it means that the infection began three to five months before testing. This is particularly useful in congenital infection, where pregnancy status and gestational age at time of infection determines treatment.

In contrast to IgG, IgM antibodies can be used to detect acute infection, but generally not chronic infection. The IgM antibodies appear sooner after infection than the IgG antibodies and disappear faster than IgG antibodies after recovery. In most cases, "T. gondii"-specific IgM antibodies can first be detected approximately a week after acquiring primary infection, and decrease within one to six months; 25% of those infected are negative for "T. gondii"-specific IgM within seven months. However, IgM may be detectable months or years after infection, during the chronic phase, and false positives for acute infection are possible. The most commonly used tests for the measurement of IgM antibody are double-sandwich IgM-ELISA, the IFA test, and the immunosorbent agglutination assay (IgM-ISAGA). Commercial test kits often have low specificity, and the reported results are frequently misinterpreted.