Knowledge-based patient screening for rare and emerging infectious/parasitic diseases: a case study of brucellosis and murine typhus.

Many infectious and parasitic diseases, especially those newly emerging or reemerging, present a difficult diagnostic challenge because of their obscurity and low incidence. Important clues that could lead to an initial diagnosis are often overlooked, misinterpreted, not linked to a disease, or disregarded. We constructed a computer-based decision support system containing 223 infectious and parasitic diseases and used it to conduct a historical intervention study based on field investigation records of 200 cases of human brucellosis and 96 cases of murine typhus that occurred in Texas from 1980 through 1989. Knowledge-based screening showed that the average number of days from the initial patient visit to the time of correct diagnosis was significantly reduced (brucellosis-from 17.9 to 4.5 days, p = 0.0001, murine typhus-from 11.5 to 8.6 days, p = 0.001). This study demonstrates the potential value of knowledge-based patient screening for rare infectious and parasitic diseases.

Protozoal abortion in a herd of cattle concurrently infected with Hammondia pardalis.

Protozoal infection was diagnosed as the cause of abortion in a large drylot dairy herd located in northeastern Mexico. Diagnosis was made on the basis of finding encephalitis, myocarditis, protozoal cysts, and protozoal tachyzoites in aborted fetuses. The blended ration fed to the cows had been contaminated by the feces of a large resident population of feral domestic cats that used components of the blended ration for den sites (stored hay) or as a latrine (grain). The cows that aborted contained tissue phases of a protozoan infective for domestic cats. The morphologic features of the oocyst and biologic features of the protozoan were identical to those of Hammondia pardalis.

Clinical and epizootiologic characteristics of dogs seropositive for Borrelia burgdorferi in Texas: 110 cases (1988).

Of 2,409 canine serum samples submitted to the Texas Veterinary Medical Diagnostic Laboratory between Jan 1, 1988 and Dec 31, 1988 and tested by immunofluorescent antibody technique for antibody to Borrelia borgdorferi, 132 (5.5%) had positive results. Clinical and epizootiologic characteristics of seropositive dogs from Texas (n = 110) were examined. Male dogs were more likely than female dogs to be seropositive for B burgdorferi. The most frequent clinical sign of disease described in seropositive dogs was lameness; neurologic, ophthalmologic, dermatologic, renal, and hepatic signs also were reported by referring veterinarians.

Epizootiologic association between feline immunodeficiency virus infection and feline leukemia virus seropositivity.

Five hundred twenty-one feline serum samples submitted to the Texas Veterinary Medical Diagnostic Laboratory between Nov 1, 1988, and Jan 31, 1989 were tested for antibody to feline immunodeficiency virus (FIV) by use of an ELISA. The prevalence of FIV infection in this population was 11.3% (95% confidence interval: 8.6 to 14.0%). Serologic test results for FeLV were available for 156 of the 521 cats. A significant (P = 0.008) association between FIV infection and FeLV seropositivity was observed; FeLV-positive cats were nearly 4 times more likely to be seropositive for FIV than were FeLV-negative cats. The association remained statistically significant (P = 0.021) after adjusting for age and gender, using multiple-logistic regression analysis.

Treatment of giardiasis in adult Greyhounds, using ipronidazole-medicated water.

Two of 3 adult Greyhounds with clinical signs of giardiasis were treated by the addition of ipronidazole hydrochloride to their water supply (126 mg/L) for 7 days. Within 15 hours, the dogs had improved clinically, and large numbers of degenerating Giardia cysts were passed. After 54 hours, cyst shedding had ceased. The nontreated control dog continued to shed Giardia cysts. During an additional 7 days, the dogs were treated with ipronidazole-medicated water (378 mg/L) and remained clinically normal.

Catastrophic death losses in a dairy herd attributed to type D botulism.

Clostridium botulinum type D intoxication was diagnosed as the cause of death of 42 of 67 lactating cows in a southeast Texas dairy herd over an 11-day period. By necessity, the diagnosis was based on clinicopathologic findings, as the toxin could not, by standard laboratory tests, be demonstrated in affected cattle. The predominant clinical findings were hindlimb weakness/ataxia rapidly progressing to persistent recumbency. Affected cattle were alert until just before death, which occurred without notable agonal movements or respirations after 6 to 72 hours' recumbency. Abnormal laboratory findings included neutrophilic leukocytosis (all affected cattle), proteinuria (most affected cattle), slight elevations of serum aspartate transaminase and low serum inorganic phosphorus (some affected cattle), and patchy areas of hyperemia/congestion of the mucosa in the small intestine (postmortem examination of 3 affected cattle). This report confirms the findings of others with regard to the difficulty of demonstrating the causative toxin in C botulinum type D-intoxicated cattle and presents available information on the clinicopathologic features of this intoxication that may aid in the differentiation of this condition from other causes of down cows.

Studies on canine parvovirus infections: development of an inactivated vaccine.

parvoviruses isolated from the intestines of dogs that died of an enteric infection were propagated in various parasynchronized canine and feline cell cultures. Viral antigen could be visualized in infected cell cultures with the aid of fluorescein-labeled feline, as well as porcine, parvovirus antisera, and in an indirect test with sera from dogs that had recovered from a parvovirus infection. The virus hemagglutinated porcine RBC at 4 C and 25 C but not at 37 C. An inactivated canine parvovirus vaccine elicited an immune response, but no adverse reactions, when inoculated into dogs. Vaccinated dogs were immune and did not show any clinical signs when challenge exposed with virulent virus, whereas nonvaccinated, nonimmune dogs became clinically ill when inoculated with the same virus. Humoral hemagglutination-inhibiting parvovirus antibody values corresponded well with susceptibility and resistance to experimental inoculation of dogs with canine parvoviruses.

Myocarditis induced by parvoviral infection in weanling pups in the United States.

In a nationwide survey from January 1978 through September 1979, acute parvovirus-induced myocarditis was identified in 76 of 147 (52%) pups in 19 litters. The affected pups were from 12 states. Birth of all pups registered with the American Kennel Club during this period increased during the spring months, peaking in May, which was correlated in 4 to 8 weeks with the greatest number of cases in the study. Serologic data available for 4 dams, for 6 of their surviving pups, and for 3 contact pups indicated that all had been exposed to parvovirus. In 2 kennels, cases of acute myocarditis were preceded within 2 months by cases of severe gastroenteritis in older litters on the same premises.

Rotavirus (reovirus-like) infection of neonatal ruminants in a zoo nursery.

An outbreak of a pneumoenteric disease occurred in neonates in a zoo nursery. Four of seven affected animals died. Rotaviruses were observed in the feces of an affected 4-day old impala (Aepyceros melampus), a Thomson's gazelle (Gazella thomsonii) and an addax (Addax nasomaculatus). Encapsulated Escherichia coli also were isolated from the feces. The recovered rotaviruses was antigenically related to bovine rotavirus. A bovine rotavirus vaccine was given orally and no adverse effects were noted.

Urogenital infection and seminal excretion after inoculation of bulls and rams with chlamydiae.

Five mature rams and 4 bulls were inoculated parenterally with bovine or ovine chlamydial strains of type 1 and 2. One to 3 days later, all animals developed a chlamydemia lasting 4 to 8 days. Chlamydial agents were isolated from the semen near the end of the chlamydemic phase. All rams and 3 of 4 inoculated bulls excreted chlamydiae in the semen for 22 to 29 days. From 8 to 39 days after inoculation, selected rams or bulls were killed to test for chlamydial infection in the urogenital tract and other organs. Chlamydiae were isolated in developing chicken embryos from testis, epididymis, and accessory sex glands. Bulls examined 29 and 39 days after inoculation did not harbor chlamydiae. Chlamydiae were also not isolated from 3 control bulls which were from the same herd as the principal bulls. All inoculated bulls and rams had a group-specific chlamydial antibody response within 7 days. The titers reached maximal levels of 128 to 512 at 14 days after inoculation. Subsequently, the antibody titers decreased gradually. Seminal plasma collected at different times after animals were inoculated did not fix complement in the presence of chlamydial group antigen. The number of polymorphonuclear leukocytes in the semen increased during the experiment. The semen was grossly purulent in 2 rams inoculated with the type 2 chlamydial strain of polyarthritis.